REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

Therapy

Benzodiazepines

Benzodiazepines (BZDs) act by modulating the binding of GABA to the GABA‐A receptor, increasing the influx of chloride ions and providing an inhibitory effect which is similar to that of ethanol. Therefore, BZDs replace the repressive effect of ethanol that has been discontinued in AWS. Most BZDs are extensively and rapidly absorbed after oral administration, with bioavailability varying from 80% to 100%. They rapidly penetrate the blood–brain barrier, although the diffusion rate into the brain and other tissues varies and is largely determined by lipophilicity. All BZDs are metabolized in the liver by oxidation and/or glucuronidation, and some of them form pharmacologically active metabolites that are responsible for the long duration of action, such as diazepam, chlordiazepoxide, and clorazepate. Therefore, the BZDs and their active metabolites may be categorized according to the duration of their effect: short acting (<10 h like lorazepam, oxazepam, and midazolam), intermediate acting (10–24 h as clonazepam), or long acting (>24 h; clobazam, clorazepate, and diazepam).. The metabolism of BZDs is primarily catalyzed by CYP isoenzymes which may be the target of drug–drug interactions, sometimes leading to paradoxical effects or over sedation. When associated with paradoxical excitement, BZDs may contribute to seizure exacerbation when tapered, particularly after prolonged use.

BZDs are currently recognized as first‐line treatment for AWS. Their effectiveness to significantly reduce the risk of recurrent seizures related to alcohol withdrawal compared to placebo has been demonstrated many years ago. Nevertheless, the available evidence does not suggest that benzodiazepines are clearly superior to other drugs with the exception of a possible advantage in seizure control and prevention when compared to non‐anticonvulsants and placebo. BZDs are recommended both for primary and secondary seizure prophylaxis in AWS. A structured guideline for the identification and management of alcohol‐related seizures (EFNS TaskForce, 2005) is currently being revised. Within the first 2 d of withdrawal, BZDs reduce the incidence of seizures by up to 84% and prevent the development of DT. The current literature does not suggest one BZD to be more efficacious than another, although differences in pharmacokinetic properties can guide selection. The following recommendations include agents

1. with rapid onset to control agitation symptoms
2. with long action to avoid breakthrough symptoms
3. with less dependence on hepatic metabolism to lower the risk of over sedation

Diazepam fulfills the first two aspects and represents the primary choice. Increased age and liver disease significantly impact the CYP‐dependent metabolism of medications with a 50% decline in the clearance and a four‐ to ninefold increase in terminal half‐life of diazepam with accumulation and production of side effects. Therefore, in the elderly and patients with cirrhosis or severe liver dysfunction, lorazepam or oxazepam is preferred.

Strategies for the use of BDZ

Multiple dosing strategies have been utilized in the management of AWS. When using any dosing technique, it is important to recognize the symptoms of benzodiazepine toxicity that can include respiratory depression, excessive sedation, ataxia, confusion, memory impairment, and delirium, which may be difficult to differentiate from DT .

Loading dose regimen

The “front‐loading” or “loading dose” strategy uses high doses of longer‐acting benzodiazepines to quickly achieve initial sedation with a self‐tapering effect over time due to their pharmacokinetic properties. Typically, diazepam 10–20 mg or chlordiazepoxide 100 mg doses are repeated every 1–2 h until the patient reaches adequate sedation with an average of three doses usually required. Studies found diazepam loading to significantly reduce the risk of complications, to reduce the total dose of benzodiazepines needed, and the duration of withdrawal symptoms. A further benefit of this approach is that intensive monitoring and medication administration are limited to the early period of withdrawal. As the loading dose regimen may cause sedation and respiratory depression, withdrawal severity and the clinical condition need to be monitored prior to each dose to avoid benzodiazepine toxicity. This is especially important in elderly patients and those with hepatic dysfunction.

Fixed‐dose application

The “fixed‐dose” technique implies that a certain amount of medication is administered at regular intervals. This approach may be beneficial for patients who will require medication regardless of symptoms, such as in those with a history of seizures or DT.3 Fixed‐schedule dosing is often the only way to treat patients withdrawing from alcohol with comorbid medical illnesses or SE because of inability to assess withdrawal symptoms. Other advantages are less frequent reassessments of symptoms and fewer protocol errors in comparison with the symptom‐triggered therapy.Chlordiazepoxide and diazepam remain the agents of choice because of their long‐acting nature. A ceiling dose of 60 mg of diazepam or 125 mg of chlordiazepoxide is advised per day. After 2–3 d of stabilization of the withdrawal syndrome, the benzodiazepine is gradually tapered off over a period of 7–10 d.The peril of the fixed‐dose regimen is seen in under‐ or overestimation of the total dose; the latter is often seen in patients who are still alcohol intoxicated where unpredictable interactions with BZD may emerge.

Symptom‐triggered treatment

For this approach to be successful, patients must be symptomatic and there must be regular assessment of patient’s withdrawal symptoms using a validated tool like the CIWA‐Ar scale. Therefore, this regimen requires close monitoring. For this reason, the technique is not applicable in non‐verbal patients, and it is not safe in patients with a past history of withdrawal seizures because they can occur even without AWS symptoms. Using CIWA‐Ar, the cutoff for beginning treatment is a score of at least 8 resulting in the application of 5–10 mg diazepam or 25–100 mg chlordiazepoxide. Assessment should be repeated 1 h later. If symptoms persist, doses are repeated hourly until the score is below 8. Once stable, patients can be assessed every 4–8 h for additional therapy. The symptom‐triggered approach is as efficacious as the fixed‐dose method in managing alcohol withdrawal in terms of efficacy and incidence of adverse events.The advantages of symptom‐triggered therapy are shorter duration of detoxification, lower doses of BZD required, less sedation, and decreased risk of respiratory depression.

Non‐benzodiazepines

Antipsychotic agents

Although they may reduce symptoms of withdrawal, antipsychotics including phenothiazines and butyrophenones, like haloperidol, are associated with higher mortality due to cardiac arrhythmia by prolongation of the QT interval. Furthermore, they lower the seizure threshold. Therefore, antipsychotic agents should be used cautiously in AWS, particularly in its early stage (<48 h) when the seizure risk is high. Nevertheless, they may be considered as adjunctive therapy to benzodiazepines in the late stage of AWS, when agitation, delirium, and hallucinations are not controlled with BZD alone.

Antiepileptic agents

Seven randomized controlled studies, including over 600 patients, have investigated the effectiveness of carbamazepine (CBZ) in comparison with BZD. At daily doses of 800 mg with either a fixed or a tapered regimen over 5–9 d, CBZ was well tolerated and reduced withdrawal symptoms. Nevertheless, due to underenrollment, delayed medication administration, insufficient sample size, and inadequate dosage, the impact of CBZ to prevent seizures or DT is still uncertain and effectiveness compared to BDZ has not been verified. A retrospective analysis of over 700 patients comparing CBZ to valproate (VPA) found VPA to offer some benefits compared to CBZ, such as favorable tolerability and shorter duration of treatment. However, because of the study design and the lack of comparison to BZD, the study did not support implementation into clinical routine. Concerning gabapentin, there were similar results with some effects on mild/moderate withdrawal symptoms but no superiority to BZD.

As levetiracetam (LEV) has no significant affinity to GABAergic and glutamatergic receptors, its mechanism of action in AWS is still unclear. LEV represents a pyrrolidine derivate with binding to the synaptic vesicle protein SV2A, hereby regulating calcium‐dependent neurotransmitter release. Thus, it might reduce excessive neuronal activity and may exert neuroprotective effects. Due to its high tolerability and advantageous pharmacokinetics with lack of drug–drug interactions, LEV appears to be a promising agent in the therapy of AWS. The few available data have shown that the treatment with LEV resulted in a rapid and stable clinical improvement of AWS. Its usefulness in AWS treatment still needs to be investigated.

In summary, besides BZD, anticonvulsants seem to be widely used for the treatment of AWS. Nevertheless, a Cochrane review investigating 56 studies with a total of 4076 participants found no sufficient evidence in favor of any antiepileptic agent for therapy of AWS.

Alpha‐2 agonistic agents

Dexmedetomidine (DEX), a more potent ɑ‐2 agonist than clonidine, decreases sympathetic overdrive and release of norepinephrine. Due to its rapid onset of action and short half‐life, it produces a “cooperative sedation” without necessity for intubation. As ɑ‐2 agonists lack the GABAergic activity to prevent and treat DT or seizures, they can only be used as adjunctive therapy to reduce autonomic hyperactivity that cannot be controlled by BZD alone. Several studies demonstrated a BZD‐sparing effect with significant reduction in BZD requirement.

Anesthetic agents

Propofol

Propofol enhances the inhibitory effects at the GABA‐A receptor and decreases excitatory circuits of the NMDA transmitter system. Due to its strong lipophilic properties, it features a rapid onset of action and is easy to titrate because of the short half‐life. Propofol has general anesthetic effects that often require intubation and mechanical ventilation. Its use is therefore restricted to the intensive care unit making this agent an adjunct therapy for refractory cases of AWS.Its application and experience in AWS is limited to only a few cases and rebound of withdrawal symptoms soon after stopping propofol infusion has been reported.

Barbiturates

Barbiturates are also GABA‐enhancing drugs that work synergistically with BZD featuring a different receptor profile. They can be given orally or intravenously with a loading dose of 100–200 mg/h and have been shown to be as effective as BZD. Unfortunately, barbiturates have a narrow therapeutic index with a long half‐live making titration difficult. They increase the likelihood of respiratory insufficiency and coma so that intubation and mechanical ventilation is often necessary. Because there is no antidote to toxicity, barbiturates are not used frequently in the therapy of AWS.

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

Others

Clomethiazole

As the parenteral form of clomethiazole is no longer available, its application is dependent on sufficient alertness and cooperation to enable peroral treatment. For adequate alleviation of delirious symptoms, 200 mg capsules are administered (maximum 24 capsules per day) and doses are repeated every 2–3 h until sufficient calming. As with BZDs, CNS respiratory center depression may emerge, especially in combination with BZDs, whose daily doses should be reduced to 15–20%. Further side effects of clomethiazole are an increased risk of pneumonia due to bronchial mucus accumulation as well as dependence, so that administration should not exceed 10 d. Moreover, clomethiazole is subjected to a pronounced first pass effect by the isoenzyme CYP2E1 which is blocked by ethanol consumption. Accordingly, the combinatory intake of clomethiazole and ethanol should be avoided due to its possible life‐threatening effects.

Gamma‐hydroxybutyric acid (GHB) and Sodium oxybate (SMO)

GHB, admitted to the treatment of narcolepsy, is an endogenous neurotransmitter and a metabolite of GABA. It has a stake in GABA‐dependent neurotransmission, dopamine release, and thereby, it regulates the wake–sleep cycle. GHB acts as a depressant at higher doses and has anxiolytic properties. A Cochrane review shows impact on symptoms of alcohol withdrawal in comparison with placebo, but no superiority to BZDs or clomethiazole in prevention of AWS with a high risk of misuse, abuse, and addiction. SMO is the sodium salt of γ‐hydroxybutyric acid, a naturally occurring short‐chain fatty acid that is structurally similar to GABA. In addition to the activation of the GABA‐A receptor, it has also alcohol mimicking effects due to dopamine release in the CNS. There are some studies showing SMO to be equally effective as BZD in moderate‐to‐severe AWS.When used for a short period, SMO is relatively well tolerated; in long‐term use, there is, as is known for GHB, concern about abuse and dependence based on its euphoric properties.

Baclofen

Baclofen, a GABA‐B receptor agonist and a well‐known muscle relaxant for treatment of spasticity, has similar mechanisms of action and similar effects as SMO. Consistent with preclinical evidence, open‐label reports demonstrated the ability of baclofen to rapidly reduce symptoms of severe AWS and to decrease craving. Due to only a few trials, there is not enough evidence to recommend its use.

Adjunctive Therapeutic Agents

Magnesium

Magnesium is an important cofactor of many enzymes and acts as an inhibitor of neurotransmitter release. Therefore, it may dampen the NMDA‐driven hyperexcitability in AWS by competing with glutamate in its receptor binding site. Furthermore, magnesium impedes the NO synthase and calcium‐dependent channels, lowering action potential firing. As chronic alcohol use is associated with abnormal magnesium metabolism, patients have been given magnesium to treat or prevent AWS. Based on a Cochrane review, there is currently insufficient evidence to support the routine use of magnesium for prophylaxis or treatment of AWS. Nevertheless, as alcohol use and withdrawal are connected with QT interval prolongation and cardiac arrhythmia, laboratory values of magnesium should be determined and deficiencies be balanced.

Thiamine

Wernicke’s encephalopathy (WE) is afflicted with high morbidity and mortality and presents only in rare cases with the classic triad of confusion, ataxia, and ophthalmoplegia. According to the EFNS guideline for diagnosis of WE, two of the following four signs are required: (i) dietary deficiencies, (ii) eye signs, (iii) cerebellar dysfunction, and (iv) either an altered mental state or mild memory impairment. Particularly in severe AWS with predominant symptoms of DT, differentiation from WE is sometimes impossible. Because of its easy and uncomplicated treatment, prevention of WE with parenteral thiamine should be performed in all patients at risk, including those experiencing AWS and prior to any parenteral carbohydrate‐containing fluids. The earlier thiamine supplementation is started, the faster is recovery, regardless of initial clinical presentation.

Conclusions

Alcoholics are a diverse group. They experience different subsets of symptoms, and the disease has different origins and modulating influences for different people. Therefore, to understand the effects of alcoholism, it is important to consider the influence of a wide range of variables on a particular behavior or set of behaviors. The underpinnings of alcohol-induced brain defects are multivariate; to date, the available literature does not support the assertion that any one variable can consistently and completely account for these impairments. Instead, the identification of the most salient variables is a primary focus of current research. In the search for answers, we recommend an integrative approach that recognizes the interconnectivity of the different functional systems to account for the heterogeneity of outcome variables associated with alcoholism-related impairments and recovery of functions. It is helpful to use as many kinds of tools as possible, keeping in mind that specific deficits can be observed only with certain methods, with rigorous paradigms, and with particular groups of people with distinct risk factors. Such confluence of information can provide evidence linking structural damage, functional alterations, and the specific behavioral and neuropsychological effects of alcoholism. These measures also can determine the degree to which abstinence and treatment result in the reversal of atrophy and dysfunction.

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

INTRODUCTION-

Alcoholism results from an interplay between genetic and environmental factors, and is linked to brain defects and associated cognitive, emotional, and behavioral impairments. A confluence of findings from neuroimaging, physiological, neuropathological, and neuropsychological studies of alcoholics indicate that the frontal lobes, limbic system, and cerebellum are particularly vulnerable to damage and dysfunction. An integrative approach employing a variety of neuroscientific technologies is essential for recognizing the interconnectivity of the different functional systems affected by alcoholism. In that way, relevant experimental techniques can be applied to assist in determining the degree to which abstinence and treatment contribute to the reversal of atrophy and dysfunction.

The alcohol withdrawal syndrome is a well‐known condition occurring after intentional or unintentional abrupt cessation of heavy/constant drinking in patients suffering from alcohol use disorders (AUDs). AUDs are common in neurological departments with patients admitted for coma, epileptic seizures, dementia, polyneuropathy, and gait disturbances. Nonetheless, diagnosis and treatment are often delayed until dramatic symptoms occur. The purpose of this review is to increase the awareness of the early clinical manifestations of AWS and the appropriate identification and management of this important condition in a neurological setting.

An estimated 76.3 million people worldwide have alcohol use disorders (AUDs), and these account for 1.8 million deaths each year. It is estimated that up to 42% of patients admitted to general hospitals, and one‐third of patients admitted to hospital intensive care units (ICU) have AUD. Alcohol withdrawal syndrome (AWS) is a well‐known condition occurring after intentional or unintentional abrupt cessation of heavy/constant drinking, and it occurs in about 8% of hospitalized AUD inpatients. Severe AWS more than doubles the length of stay and frequently requires treatment at the ICU. A complicated AWS includes epileptic seizures and/or delirium tremens (DT), the occurrence of which may be as high as 15% in AUD patients., Delirious patients show high rates of comorbidities, and their mortality rate is comparable to patients having severe malignant diseases. However, with early detection and appropriate treatment, the expected mortality is in the range of 1% or less.

AUDs are common in patients referred to neurological departments, admitted for coma, epileptic seizures, dementia, polyneuropathy, and gait disturbances. Nonetheless, diagnosis and treatment are often delayed until dramatic symptoms occur. The purpose of this review is to increase the awareness of the early clinical manifestations of AWS and the appropriate identification and management of this important condition in a neurological setting.

Types of Alcohol-Related Neurologic Disorders

There are several neurological diseases that can be caused by alcohol abuse, including fetal alcohol syndrome, dementia, and some symptoms associated with alcohol withdrawal. Alcohol-related neurological diseases include:

• Alcoholic cerebellar degeneration: This is one of the more common forms of cerebellar ataxia, or loss of tissue mass in the brain. The most common symptom associated with cerebellar degeneration involves the loss of the ability to walk over a period of months or years. The condition also affects eye movements, gait or pace, and, rarely, loss of muscle coordination in the upper body. Cerebellar degeneration is caused by malnutrition, but the main cause in most of the Western world is alcohol abuse.
• Alcoholic myopathy: About 33 percent of people struggling with alcohol use disorder develop alcoholic myopathy. This condition involves the breakdown of proximal muscles, which are found in the arms, shoulders, thighs, and upper legs – skeletal muscles found nearest the body’s trunk. Symptoms include:
  • Muscle pain, tenderness, swelling, and weakness, which may appear after a binge or when the person wakes from an alcoholic stupor
  • Cardiomyopathy, or weakening and drooping of the heart muscle so it does not pump blood efficiently
  • Renal damage or failure, when the toxins from muscle breakdown flood the kidneys to the point that the organs can no longer effectively filter them out

Alcoholic neuropathy: Although it is unclear what exactly causes the condition, alcoholic neuropathy is a deadening of nerves throughout the peripheral nervous system, so the person will feel tingling or burning sensations and numbness, and have trouble with basic functions like walking, internal body temperature regulation, and bowel or bladder function. The causes of alcoholic neuropathy likely involve poisoning of the nerves due to high-volume consumption of alcohol and poor nutrition associated with problem drinking. Symptoms of alcoholic neuropathy include:

• Numbness in the extremities, including the arms and legs
• The feeling of “pins and needles” or other abnormal sensations
• Pain or burning in the arms and legs
• Muscle problems, including cramps, weakness, spasms, or aching sensations
• Heat intolerance due to poor regulation, especially after exercise
• Incontinence, trouble urinating, or other bladder problems
• Diarrhea or constipation
• Nausea and vomiting
• Trouble speaking or swallowing
• Unsteady gait, stumbling, or lack of balance

Delirium tremens: When a person suddenly stops drinking after abusing alcohol for many years, they are at risk of developing alcohol withdrawal syndrome, or delirium tremens (DT). The body has developed a physical dependence on alcohol to manage brain function, so when the substance is suddenly removed, life-threatening side effects can develop. These include:

• Severe confusion or delirium
• Physical tremors
• Changes in thinking or memory
• Extreme agitation and irritability
• Intense excitement, fear, or paranoia
• Hallucinations
• Sudden bursts of energy
• Stupor, or being awake but unresponsive
• Seizures or convulsions

Fetal alcohol spectrum disorders: While many alcohol-related neurological conditions occur in people who consume too much alcohol, fetal alcohol spectrum disorders (FASDs) occur in babies or children, and may lead to life-long developmental delays, emotional or behavioral abnormalities, or trouble thinking or learning. Women who consume alcohol while pregnant put their children at risk for FASDs. Types of FASDs include:

• Fetal alcohol syndrome (FAS): Fetal death is the most extreme outcome from a woman struggling with AUD or problem drinking during pregnancy; other forms of FAS include abnormal facial features, growth problems, and developmental differences or disabilities in the central nervous system (CNS). People who live with FAS may have trouble with their memory, attention, communication skills, learning abilities, hearing, and/or vision.
• Alcohol-related neurodevelopmental disorder (ARND): With this disorder, children and adults have intellectual disabilities, behavioral struggles, and trouble learning.
• Alcohol-related birth defects: These involve physical problems, including damage to the heart, kidneys, hearing, or bones during fetal development.

Wernicke-Korsakoff syndrome: This condition is a combination of two forms of brain disease, Wernicke’s encephalopathy and Korsakoff syndrome. Both of these conditions are triggered by a loss of thiamine, or vitamin B12, which is most often caused by problem drinking. When a person struggles with heavy drinking or alcohol use disorder, they are more likely to drink alcohol than eat regular meals, and the body will struggle to absorb nutrients from food over time.Symptoms of Wernicke’s encephalopathy include:

• Reduced mental activity
• Confusion
• Ataxia, starting with muscle tremors in the legs and leading to loss of muscle control overall
• Abnormal eye movements
• Double vision
• Eyelid drooping
• Withdrawal symptoms if the person stops drinking

Korsakoff syndrome’s symptoms include:

• Trouble forming new memories
• Trouble remembering old memories, leading to fabrication of events or people
• Other forms of severe memory loss
• Hallucinations, especially visual or auditory

In some cases, one or both syndromes will clear up on their own; however, in 25 percent of Wernicke-Korsakoff syndrome cases, the problem does not stop on its own and is likely to get worse. This is especially true if the person does not stop drinking alcohol and get treatment.

Pathophysiology

Ethanol is a central nervous system depressant that produces euphoria and behavioral excitation at low blood concentrations due to increased glutamate binding to N‐methyl‐D‐aspartate (NMDA) receptors; at higher concentrations, it leads to acute intoxication by potentiation of the gamma‐aminobutyric acid (GABA) effects, particularly in receptors with delta subunits. The local distribution of these subunits explains why the cerebellum, cortical areas, thalamic relay circuitry, and brainstem are the main networks that mediate the intoxicating effects of alcohol. Prolonged alcohol use leads to the development of tolerance and physical dependence, which may result from compensatory functional changes by downregulation of GABA receptors and increased expression of NMDA receptors with production of more glutamate to maintain central nervous system (CNS) transmitter homeostasis.

Abrupt cessation of chronic alcohol consumption unmasks these changes with a glutamate‐mediated CNS excitation resulting in autonomic overactivity and neuropsychiatric complications such as delirium and seizures. The latter are usually of generalized tonic–clonic type and are mediated largely in the brainstem by abrogation of the tonic inhibitory effect of the GABAergic delta subunits. Therefore, the trigger zone of these seizures is distinct from that believed to be responsible for seizures in the context of epilepsy, and this may explain why epileptiform activity is rarely observed in the EEG after alcohol withdrawal seizures. As upregulation of NMDA receptors as well as reduced GABA‐A receptor inhibition largely explain the clinical symptoms, the therapeutic approach to AWS mainly targets these mechanisms. Dopamine is another neurotransmitter involved in alcohol withdrawal states. During alcohol use, increase in dopamine positively influences the reward system thereby maintaining abuse. In withdrawal, increase in dopamine levels contributes to the clinical manifestations of autonomic hyperarousal and hallucinations. Moreover, polymorphisms in the dopamine receptor 2 gene seem to influence not only AUD but also the clinical manifestation of alcohol withdrawal symptoms. In combination with increased glutamate and norepinephrine, it may also cause the elongation of the QT interval in people who have active epilepsy; this can increase the risk of sudden unexpected death in epilepsy (SUDEP).Another excitotoxic compound that is increased in AUD is homocysteine. During active drinking, there is an increase in homocysteine through stimulation of the NMDA receptors. In withdrawal, excitotoxicity is induced by further raise in homocysteine via rebound activation of glutamatergic neurotransmission.

Clinical spectrum

AWS represents a group of symptoms that usually arise 1–3 d after the last drink. Sometimes, the symptoms are already present when the alcohol blood level is above 0 (0.5‰ or even more). The Diagnostic and Statistical Manual of Mental Disorders (DSM‐5) outlines diagnostic criteria for AWS using two main components so that the AWS is diagnosed when the following two conditions are met:

1. A clear evidence of cessation or reduction in heavy and prolonged alcohol use.
2. The symptoms of withdrawal are not accounted for by a medical or another mental or behavioral disorder.

Autonomic symptoms	Motor symptoms	Awareness symptoms	Psychiatric symptoms
Tachycardia	Hand tremor	Insomnia	Illusions
Tachypnea	Tremulousness of body	Agitation	Delusions
Dilated pupils	Seizures	Irritability	Hallucinations
Elevated blood pressure	Ataxia	Delirium	Paranoid ideas
Elevated body temperature	Gait disturbances	Disorientation	Anxiety
Diaphoresis	Hyper‐reflexia		Affective instability
Nausea/vomiting	Dysarthria		Combativeness
Diarrhea			Disinhibition

The alcohol withdrawal syndrome is a dynamic and complex process. For this reason, there have been many attempts to classify symptoms of AWS either by severity or time of onset to facilitate prediction and outcome. In early stages, symptoms usually are restricted to autonomic presentations, tremor, hyperactivity, insomnia, and headache. In minor withdrawal, patients always have intact orientation and are fully conscious. Symptoms start around 6 h after cessation or decrease in intake and last up to 4–48 h (early withdrawal, Hallucinations of visual, tactile or auditory qualities, and illusions while conscious are symptoms of moderate withdrawal. They can last up to 6 d. The appearance of acute symptomatic seizures may emerge 6–48 h after the last drink. Delirium tremens (DT, onset 48–72 h after cessation of drinking) represents characteristics of severe withdrawal that may last for up to 2 weeks (late withdrawal)

The alcohol withdrawal seizure is a symptom occurring primarily during the early phase of withdrawal and is characterized by reduction in the seizure threshold. More than 90% of acute symptomatic seizures emerge within 48 h of cessation of prolonged drinking. Seizures frequently occur in the absence of other signs of the AWS. More than half of the individuals present with repeated seizures, and in up to 5%, they may progress to status epilepticus. More than 50% of withdrawal seizures are associated with concurrent risk factors such as prior epilepsy, structural brain lesions, or use of other drugs. It is remarkable that the development of acute symptomatic seizures during an alcohol withdrawal episode is associated with a fourfold increase in the mortality rate that is due to complications of severe AUD rather than a direct effect of seizures. The appearance of a withdrawal seizure represents a strong risk factor for progression into a severe withdrawal state with following development of DT in up to 30% of cases. Unprovoked seizures occurring later than 48 h after the last drink suggest other causes such as head trauma or combined drug withdrawal effects.

Delirium is a clinical syndrome of acute onset characterized by a global confusional state, perceptual abnormalities, and somatic symptoms of vegetative or central nervous presentation. Hallucinosis represents a unique form of withdrawal‐related psychosis which can begin even while the person is continuing to use alcohol or after cessation of drinking. The sensorium is clear in the beginning, but it often evolves into the syndrome of DT, a specific type of delirium typically associated with psychomotor agitation (hyperactive delirium) which emerges during the late withdrawal phase. Delirium can also manifest as a hypoactive state with decreased arousal and psychomotor activity, which is associated with a worse prognosis, delayed diagnosis and treatment as well as later complications. In cases of hypoactive delirium, comorbid or other medical illnesses must be ruled out. This is especially important in patients who have not had a previous history of DT.

Hyponatremia	Due to poor oral intake, dehydration, and uremia; frequently presenting as hypoactive delirium
Hepatic encephalopathy	Jaundice, hematemesis, melena, icterus, flapping tremor, ascites, sleep–wake reversal
Pneumonia	Fever, cough, low arterial blood oxygen saturation, delirium before cessation of alcohol use
Encephalitis/Meningitis	Fever, meningeal signs, and focal neurological deficits; MRI/CSF abnormalities
Head injury	Being found unconscious, ear or nose bleeding, pinpoint pupils, focal neurological deficits
Thyrotoxicosis	History of thyroid illness; thyromegaly, exophthalmos, lagophthalmos
Lithium intoxication	History of psychiatric illness, drug overuse, diarrhea, fever, use of NSAID or diuretics
Atropine/Tricyclic intoxication	Fever, hot dry skin, dilated pupils
Psychosis	Hallucinations/delusions of long‐standing duration, absence of clouding of sensorium
Antidepressant intoxication	Use of SSRI; diarrhea, myoclonus, jitteriness, seizures, altered sensorium
Subacute encephalopathy with seizures in AUD	Several days after alcohol cessation; complex/simple partial seizures with reversible motor deficits; in EEG focal slowing, periodic lateralized discharges; MRI with reversible T2w flair hyperintensities

In summary, physical examination and investigations should be directed toward detecting signs of intoxication, seizures, hallucinations, and delirium tremens as well as Wernicke’s encephalopathy (one or more symptoms of ataxia, amnesia, and ophthalmoplegia). Apart from neuropsychiatric symptoms, physical injury or medical problems including aspiration pneumonia, dehydration, and electrolyte imbalance should be taken into account.

Biomarkers

In several studies, possible predictors for the development of a severe AWS have been investigated. Medical history and laboratory biomarkers are the two most important methods for the identification of patients at high risk. It appears that the most robust predictor for an incident occurrence of DT or seizures is a history of a similar event.Clinical findings such as elevated heart rate, systolic blood pressure, and temperature are all easily verifiable in the initial patient assessment, although their predictive value to identify patients with AWS who are more likely to develop DT is not high. In a patient with impaired consciousness, laboratory markers represent helpful tools to confirm the suspected clinical diagnosis of an AUD.

Markers useful in the emergency setting

The quantitative, measurable detection of drinking is important for the successful treatment of AUD. Therefore, the importance of direct and indirect alcohol markers to evaluate consumption in the acute clinical setting is increasingly recognized. he detection of ethanol itself in different specimens is still a common diagnostic tool to prove alcohol consumption. Alcohol ingestion can be measured using a breath test. Although ethanol is rapidly eliminated from the circulation, the time for detection by breath analysis is dependent on the amount of intake as ethanol depletes according to a linear reduction at about 0,15‰/1 h. Alcohol use can alternatively be detected by direct measurement of ethanol in blood or urine. The time course of the ethanol concentration in the blood after the ingestion of an alcoholic beverage is controlled by its pharmacokinetics that represents an interplay between the kinetics of absorption, distribution, and elimination and is thus important in determining the pharmacodynamic responses to alcohol. There is a large degree of variability in alcohol metabolism as a result of both genetic and environmental factors.

Ethanol	BreathBloodUrine	<6 h	5–24 hdepletion 0,15‰/1 h	~ 90%/~ 95%	Conversion factor breath alcohol:blood alcohol 1:2100 within 2–5 h after the last drink
Hypokalemia	Blood	<6 h	Days to weeks	~ 47%/~ 90%	Serum levels <2,5 mmol/L indicate severe AUD
Thrombocytopenia	Blood	<6 h	7–12 d	~ 69%/~ 75%	High NPV, low PPV; rebound thrombocytosis after cessation of alcohol abuse
Mean corpuscular volume	Blood	<6 h	4 mo	~ 80%/~ 60%	Dose‐dependent increase
γ‐glutamyltransferase	Blood	<6 h	2–8 wk	~ 80%/~ 65%	Severe AUD with liver damage
Ratio AST/ALT >2	Blood	<6 h	AST 18 hALT 36 h	~ 50%/~ 80%	Severe AUD, marker of liver damage

Apart from ethanol itself, indirect markers of AUD are widely available and mostly part of routine laboratory testing. Severe AWS involves changes in electrolytes, especially potassium that is due to increased catecholamine activity with activation of the sodium–potassium ATPase pump and elevated vasopressin. Hypokalemia is not specific for alcohol consumption but is frequently reported to be associated with DT or seizures. The same applies to thrombocytopenia (with high negative predictive value) that additionally is predictive of an incident occurrence of DT and seizures. More indirect markers, such as AST, ALT, γGT, and MCV, are widely available and relatively inexpensive, but their predictive value is restricted because of low specificity. The interpretation of elevated values has to take into account other influencing factors including gender, age, comorbid disorders, and medication that also may increase these markers.

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

Additional markers to detect AUD

Further biomarkers for non‐emergency cases or in the event of forensic questions are listed in Table . Carbohydrate‐deficient transferrin (CDT) is the most available and studied biomarker and has a high specificity for severe AUD. CDT values are not markedly influenced by medications except by immunosuppressants. The main disadvantage is the relatively low sensitivity making this parameter unsuitable as a screening tool. As CDT, γGT, and MCV are connected with AUD by different pathophysiological mechanisms, a combination of these parameters will further improve their diagnostic value.

Carbohydrate‐deficient transferrin	Blood	>6 h	2–4 wk	~ 98%/~ 70%	Severe AUD	24, 37
Ratio γGT:CDT	Blood	>6 h	2–3 wk	~ 92%/~ 84%	Severe AUD	24, 32
Ethylglucuronid	Bloodurinehair	>6 h	8 h20–80 h3 mo	~ 99%/~ 89%	Values dependent on creatinine clearance	31, 37
Ethylsulfate	Bloodurine	>6 h	8 h36–78 h	~ 99%/~ 89%	Values dependent on creatinine clearance	31, 37
Phosphatidylethanol	Blood	>6 h	4 wk	~ 99%/~ 98%	Detection also available for dry blood spots	27, 31, 42, 53
Fatty acid ethyl esters	Bloodhair	>6 h	24 h3 mo	~ 97%/~ 77%	Combined measurement of ethylglucuronide and fatty acid ethyl esters in hair increases accuracy of interpretation	27, 31, 44, 54
5‐hydroxytryptophol:5‐hydroxyindole‐3‐acetic acid	Urine	>6 h	24 h	~ 99%/~ 77%	Ratio >20 marker for recent alcohol intake	47, 48
Whole blood acetaldehyde	Blood	>6 h	4 wk	~ 93%/~ 78%	False‐positive results in diabetics	55
Total sialic acid	Blood	>6 h	Several weeks	~ 95%/~ 81%	Glycoconjugate metabolite	37, 44, 56
Homocysteine	Blood	>6 h	Several weeks	~ 61%/~ 72%	Cutoff ~24 μmol

Apart from indirect markers for AUD, more specific alternatives focus on metabolic markers comprising direct products of alcohol degradation, that is, phosphatidylethanol (Peth), ethylglucuronide (EtG), ethylsulfate (EtS), and fatty acid ethyl esters (FAEE). Their presence is closely connected to alcohol consumption, and the well‐known CDT as well as sialic acid and EtG are the result of alcohol‐induced glycoconjugate metabolites. The highest sensitivity of up to 99% was observed for Peth that showed a rapid decrease at the beginning of withdrawal, a slow decline after the first few days, and persistence at low levels beyond 19d of abstinence. Apart from biomarkers detected in blood and urine samples, saliva is a promising and easy accessible material to detect glycomarkers of oxidative stress, but the reproducibility and validity in Peth has to be proven for clinical routine application. As an antibody based flash test is available for detection of EtG in urine with good sensitivity and specificity, this parameter is the most promising one to be integrated in routine laboratory settings and in screening of patients at risk to develop AWS.

As long as ethanol is metabolized, the metabolism of serotonin is shifted from formation of 5‐hydroxyindole‐3‐acetic acid (5‐HIAA) toward 5‐hydroxytryptophol (5‐HTOL). The 5‐HTOL/5‐HIAA ratio increases appreciably in urine after alcohol intake and is a promising marker for recent alcohol intake with a short window of detection. Until now, it has not found its way into clinical routine because of costly detection assays.

Recent investigations pointed out that homocysteine levels on admission might be a useful screening method for the risk of seizures in AWS, particular in combination with CDT. Several days after alcohol abstinence, homocysteine plasma levels decrease to normal. Homocysteine levels are influenced by nutritional status, gender, and age. Its metabolism is dependent on the enzyme 5,10‐methylenetetrahydrofolate reductase (MTHFR). The single‐nucleotide polymorphism MTHFR C677T elevates plasma homocysteine levels. Lutz et al. investigated two groups of patients with AWS and found this polymorphism to be related to higher occurrence of withdrawal seizures in the Western European population.

ALCOHOL AT A NEUROTRANSMITTER LEVEL

Alcohol’s central nervous system (CNS) effects are mediated through actions on a variety of neurotransmitters. There is a complex interplay between excitatory and inhibitory systems . The numerous transmitters involved in alcohol’s action explain its diverse effects and the large number of drug interactions with both prescribed and illicit drugs.

Alcohol and neurotransmitters

• Dopamine: alcohol increases dopamine use in the nucleus accumbens, mediating its pleasurable effects via the common reward pathway of the mesolimbic system

• Noradrenaline: alcohol release of noradrenaline (norepinephrine) contributes to the enlivening and activating “party” effects of alcohol

• Endogenous opioids: Alcohol’s analgesic, pleasure, and stress reducing functions are opioid related

• GABA: Alcohol can potentiate GABA (γ aminobutyric acid) activity through certain subunits of the GABA A receptor. This accounts for alcohol’s anxiolytic and ataxic actions, and partially for amnesia and sedation.

• Glutamate: Alcohol acts to block the excitatory NMDA (N-methyl-d-aspartate) receptor, opposing glutamate causing amnesia and other cerebral depressant effects

• Serotonin: Alcohol’s stimulation of 5HT3 (5-hydroxytryptamine 3) provides the nausea associated with alcohol use. Serotonin may also be linked to the pleasurable effects of alcohol and differing brain serotonin levels may distinguish between anxious and aggressive alcohol users

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

Differential Diagnosis

• Sacrococcygeal teratomas
• Benign teratomas
• Subcutaneous lipomas
• Lymphangiomas
• Cystic teratomas
• Spinal epidural abscess
• Spinal cord masses
• Pilonidal cyst
• Inclusion dermoid
• Caudal regression syndrome

Assessment

Initial assessment of the newborn is extremely important, preferably both by a pediatrician and a neurosurgeon. Examination of head and neck involves the assessment of head size, shape, skull bones, and openness of fontanelles, lacunar skull defects and the size of the posterior fossa. Examination of the back needs assessment of the neural placode, level of the lesion, condition of the skin, extent of skin defect and associated deformities. Examination of the lower limbs for detection of the deformities of the foot and abnormalities of long bones is important. A detailed neurological examination is necessary to assess the level of motor weakness, sensory level and sphincter dysfunction.

Prenatal diagnosis

Prenatal screening for neurological abnormalities is based on ultrasound performed routinely or oriented by maternal Alpha Feto Protein (AFP) screening. It should be performed around 12, 22 and 32 weeks. Maternal serum screening can detect up to 80% cases of spina bifida and 90% cases of anencephaly. Sonography may identify up to 90% cases of myelomeningoceles. Over the last few decades, the diffusion of routine ultrasound has changed the spectrum of the neonatal neurological malformations. Gross lethal abnormalities nearly always result in termination of pregnancy, depending on the regional law system. A growing number of more subtle abnormalities including midline or posterior fossa abnormalities are being discovered. But their postnatal outcome cannot always be predicted accurately, despite the use of fetal MRI. Maternal serum screening for chromosomal abnormalities is also increasingly used. Only in select situations, amniocentesis is contributory.

Complications

Bladder dysfunction: Most patients with myelomeningocele have some degree of bladder incontinence. Preventive goals are directed toward preventing infection with the implementation of bladder drainage utilizing intermittent catheterization or indwelling catheters. Bladder stimulation has shown to improve bladder emptying and reduce infection.  

Bowel dysfunction: Myelomeningocele is associated with anal sphincter dysfunction that results in bowel incontinence. Assisted bowel emptying reduces barriers associated with social activities, including attending school and personal relationships.

Immobility: Most myelomeningocele patients have significant weakness, which results in severe ambulation deficits or paraplegia. Bracing using external orthosis can help to maximize their mobility and ensure a near-normal developmental progression. In children over 1-year-old, utilizing a standing frame can reduce the risk of osteoporosis and the formation of contractures in lower extremities. A wheelchair can provide mobility for older children and adults.

Infections: Due to a neurogenic bladder, many have urine colonization and infections. Shunts are also prone to infections. When shunts are placed, infections can occur superficially at the skin or intraabdominal, as many of these patients have multiple abdominal procedures.

Management

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

Management of these children needs multidisciplinary approaches. Complete clinical evaluation and appropriate investigations are necessary. Parents need to be counseled and informed regarding the immediate as well as long-term management strategy.

Surgical treatment

The aim of surgery is to free the placode from the surrounding abnormal skin and reposition into the spinal canal with reconstruction of the dura and coverings to prevent CSF leak and infection. The surgical technique depends on the size and the level of the lesion. The help of pediatric, orthopedic and plastic surgeons may be necessary. Several attempts for maternal fetal surgeries to improve their outcomes have been made. The role of fetal surgery for myelomeningocele is yet to be proven.

Timing of intervention primarily depends on the clinical condition of the child and the impending risks. Surgery need not be done as a compelling emergency but should be undertaken as soon as it is practical. In case of suspected meningitis or CSF infection or colonization of the wound, prophylactic antibiotics and anticonvulsants form the initial treatment. Child is nursed in an incubator; routine blood counts and serum electrolytes are monitored. Blood grouping and cross matching is done for possible transfusion. Careful assessment of body weight is essential for intraoperative management. The newborn child with myelomeningocele should have saline dressings. It is essential not to use corrosive agents, spirit or antiseptics indiscriminately over the open defects to avoid damage to the underlying exposed neural tissue.

Surgical technique

To obtain successful repair, it is essential to study the surface anatomy and its relationships to the surrounding structures. At the apex of the myelomeningocele usually, the flat neural placode is located and from its edge the remnants of the arachnoid membrane get attached at the nerve root entry zone. From this junction, the nerve roots emerge and exit through neural foramina located ventrally. They are seen through the transparent arachnoid membrane which is fused with the skin at the lateral edges of the lesion. The dura matter which is defective posteriorly is loosely adherent to the underlying soft tissue of the back and densely adherent to the bony structures underneath. Rostrally, the dura forms tube and the neural placode continues into it, which leads to functional spinal cord.

Medical Management

Medical management of the newly born child with Spina Bifida varies according to the severity of their condition. Those with Spina Bifida Occulta do not ususally require any specific treatment. Some people with Spina Bifida Occulta do not exhibit any symptoms and may only discover they have the condition when they are older after having an XRAY. Children born with myelocoele or myelomeningocoele will require surgery normally within 2-3 days of birth in order to close the gap in the spine and return the spinal cord and nerves to their original place within the spinal column. This aims to prevent infection and further damage to the exposed spinal cord and spinal nerves. Following surgery, the child will be monitored closely for signs of common pos-operative problems associated with this type of surgery, namely hydrocephalus and leaking of cerebrospinal fluid

As the infant gets older, management of incontinence will be an important role of the medical team. Effective management strategies include the use of Clean Intermittent Catheterisation (CIC) and certain drugs which can increase the storage volume of the bladder . Children can also develop constipation due to lack of bowel movements and will require the development of a bowel programme which may involve assisted evacuation of stools. However, this will be based on an individualised assessment of the child and may involve educating the family in order to ensure the programme is effectively integrated into the child’s daily routine Effective strategies in managing incontinence in children with spina bifida are extremely important in allowing them to socially integrate themselves as they get older and attend school . The management of spina bifida varies depending on the degree the individual is affected with the disease. with acquired brain injury. A cross-sectional study (August 2020) by a multidisciplinary team describing health issues and living conditions in a cohort of adults living with Spina bifida suggests the presence of a higher prevalence of urinary and faecal incontinence, pain, and overweight in adults with Spina Bifida. Persons with the condition greater than 46 years had less complicated medical conditions, better physical and cognitive functions, and higher education, independent living, and participation in society, whereas individuals < 46 years had more secondary conditions such as hydrocephalus, Chiari II malformation, tethered cord symptoms, and latex allergy. 

pina Bifida Occulta:

• There is generally no medical treatment required

Spina Bifida Meningocele:

• Surgery is often performed early after birth, but the severity of deficits after surgery depends on if there is neural tissue in the sac.  Further treatment is similar to the management listed below for myelomeningocele.

Spina Bifida Myelomeningocele:

• Generally, surgery follows within the first few days of life to close the spinal cord defect. It is crucial during this time period prior to surgery to protect the nerves that are exposed in the protruding sac. It is also important to prevent infection and additional trauma to the exposed tissues.
  
• Additional surgeries may be required to manage other problems in the feet, hips, or spine. The individuals with hydrocephalus will also require subsequent surgeries due to the shunt needing to be replaced.
  
• The level of malformation of the spinal cord and subsequent neurological defects will influence the individual’s ability to ambulate. Assistive devices may be necessary to aid the individual around the community.
  
• Due to the bowel and bladder problems that are often caused by the neural tube defect, a bowel and bladder program may be necessary. This may include catheterization or a strict bowel and bladder regimen to remain regular.
  
• The MOMS study is a trial that was done to look at the effectiveness of having fetal surgery to fix the malformation of the fetus’s spine prior to birth in comparison to waiting until after the child is born to have the surgery.  The idea behind it was that neurological function tends to decrease as pregnancy progresses, so by performing the surgery in utero the baby would not be exposed to such extensive neurological deficits as it would if the surgery was performed after birth.  However, there is a safety concern for both the mother and the fetus when this fetal surgery is performed.  The success of the MOMS trial has now made fetal surgery a treatment option in some cases.

Neurogenic bladder is a common complication for people with spina bifida. It is normally treated with pharmaceuticals and intermittent catheterization; however for some patients this treatment does not suffice. New research suggests the idea of tissue engineering and neuromodulation.

Tissue engineering is used to generate new tissue to augment the bladder. Two different theories are utilized: unseeded and seeded. Unseeded “involves the incorporation of a scaffold material (synthetic or biologic) into the host organ, which is used as a template for the ingrowth of native cells that then initiate the regenerative process.” Seeded technology is similar to unseeded; however, it adds “cultured cells to the scaffold prior to implantation into the host.”

Neuromodulation modifies the innervation of the bladder so it can potentially function in a normal manner. Neuromodulation includes “non-operative measures such as transurethral electrical bladder stimulation, minimally invasive procedures such as implantation of a sacral neuromodulation pacemaker device, as well as operative measures that reconfigure sacral nerve root anatomy.”

Researchers are still in the early stages of development for this treatment option, however with advancements in technology is could prove to be a promising option for patients with spina bifida.

Physical Therapy Management

The role of the physiotherapist in the early management of children with spina bifida is extremely important as it helps the child to develop an efficient and purposeful movement that can be incorporated into everyday tasks. By optimising and maintaining mobility, this can eventually help children to become more independent as they get older. The physiotherapist will perform an initial assessment of the infants muscle strength and range of movement available at certain joints. This will allow the physiotherapist to determine which muscles are working properly and which ones are weak. This will give them a baseline measurement to use as a comparison as the child grows. This will also allow the physiotherapist to consider what problems the infant may have as they get older and what type of assistive devices or splints they may require when they begin to mobilise. The physiotherapist will specifically be involved in:

Joint Range of Motion

• In the early stages following surgery, the physiotherapist will begin passive range of motion exercises on the infant’s legs  . This will normally be performed 2-3 times a day. They will also demonstrate this technique to parents or carers so that they may continue to do these exercises as a home exercise programme when the infant is discharged. They may progress these exercises to mimic more functional movements which are related to normal everyday movement patterns. For example, whilst bending the left knee and hip, the right side will be kept straight as would happen in a normal walking pattern. These gentle exercises will help to maintain and may help increase the available range of motion available in joints where the movement restriction is mild. In those who have more pronounced restriction, the physiotherapist may advise that the number of exercise repetitions is increased and the movement is held for longer. The ultimate aim of range of motion exercises is to enable the child to learn and perform them independently as they grow up. It is important for the child to continue with these exercises because when they are moving independently, the functioning muscles may not be working through full range of motion. Passive range of motion exercises will therefore help to maintain flexibility and avoid the development of muscle tightenings known as contractures .

Muscle strength

• Altered muscle tone is a common symptom of spina bifida,therefore, physiotherapists use resistance training in order to strengthen these muscles that have been weakened. This is normally introduced when the infant is old enough to self mobilise. The physiotherapist can develop a programme of strength and endurance training which has been seen to improve functional abilities in children with spina bifida. These training programmes may involve a variety of exercises for the upper and lower limbs, as well as muscles of the trunk and can help improve upper limb strength and cardiovascular fitness .

Positioning and Handling

• Following the first few days after surgery, the infant will normally be placed inside or stomach lying. As the infant begins to stabilise and recover from surgery, the physiotherapist will offer advice as to how to hold the newborn child safely. This is incredibly important as the infant will have undergone major surgery which requires careful handling and positioning at all times. It may be advised that parents or carers hold the child underneath the stomach and across their forearm due to the surgical wound that will be present on the infant’s back. This handling technique may be used when sitting or walking around. When advised, parents or carers may take the infant for a walk around the hospital resting over the shoulder. This can encourage the child to begin to lift his or her head and begin to develop head and neck control .

Mobility and Ambulation

• Mobility problems in children with spina bifida can vary according to the level of the spine that has been affected during development . A child with a lesion in the lower back (Lumbar or Sacral levels), is more likely to be able to independently mobilise than one with a lesion in the upper thoracic spine. This can determine whether the child will require a wheelchair, orthotics or assistive devices.
• Parents and carers are often discouraged from using assistive devices such as infant walkers, jumpers and bouncer chairs as these can delay motor development. Infants require active movement and sensory information from the surrounding environment in order to learn how to move efficiently against gravity and maintain erect sitting and standing postures. This is no different for children with Spina Bifida. Infants with spina bifida benefit from movements that challenge control of the head, neck and torso, rather than the use of passive sitting devices or chairs. Active movement allows them to participate in the learning process. For example, rather than using a walker, parents are advised to physically hold their child in the standing position with as little support as possible to promote the necessary control of the legs and torso. This also allows the child to receive feedback from the floor and the surrounding environment .
• As the child begins to mobilise and ambulate more independently, he or she may be fitted for braces or splints to address any deformities caused by muscle imbalance or joint limitations. Orthoses such as braces and splints are supportive devices aimed at optimising existing muscle function and giving support where the child requires it. The earlier these are fitted and provided, the earlier the child will be prepared for the upright position required of standing and walking. It therefore also enhances normal developmental progression and will eventually help the child take part in normal activities of their age group . Children with Spina Bifida lesions in the upper thoracic regions of the spine may require bracing or splinting of the whole leg up to the level of the hip and chest. This is known as a Hip-Knee-Ankle-Foot Orthoses (HKAFO). Others may require orthotics aimed at stabilising the knee, ankle and foot. These are known as Knee-Ankle-Foot orthoses (KAFO) and Ankle-Foot Orthoses (AFO) Reciprocal Gait Orthoses (RGO) may be also provided in order to promote a normal rhythmic walking pattern in the child Children may require the additional use of crutches along with orthoses in order to take some stress off the legs. and standing frames are also used to help children with more severe limitations bear weight through their legs and maintain a full range of motion at all lower limb joints . Furthermore, some children may require casting as a way of treating and preventing contractures. Casting aims to develop a gradual increase in the range of motion available at a certain joint and is a very effective method of improving range of motion at tight joints without the use of surgery . Other children may benefit from the use of a wheelchair, as it can give them more freedom of movement if their walking is limited and strenuous. This can be alternated with the use of orthosis for shorter distances. A wheelchair can also help children keep pace with other able-bodied people, and enable them to participate in recreational activities at school .

Parent/carer education

• Physiotherapy management will eventually be handed over to the parents or carers of the infant. Initially they will be encouraged to observe the physiotherapist carrying out ra ange of motion exercises and handling and positioning strategies before being asked to duplicate these treatments independently. Following these teaching sessions, certain roles will then be handed over to the parents and carers. Following discharge home and as the child begins to mobilise more independently the parents and carers should actively become involved in assessing their child’s progression through observations at home when playing, sitting, crawling etc. This can help with early identification of any differences in the child’s movements or sitting postures between the home and the hospital. It may also allow other possible problems to be identified early on so that a management strategy may be developed. This is essential particularly later on when the child becomes more medically stable, as they will not receive as much medical input and interaction as when the child was a new orn infant in hospital
• The physiotherapist, along with other members of the healthcare team, will be able to offer advice and help parents and carers build confidence in their ability to manage their child’s daily routine

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

INTRODUCTION-

Spinal cord development occurs through three consecutive periods of gastrulation, primary nerulation and secondary neurulation. Aberration in these stages causes abnormalities of the spine and spinal cord, collectively referred as spinal dysraphism. They can be broadly classified as anomalies of gastrulation (disorders of notochord formation and of integration); anomalies of primary neurulation (premature dysjunction and nondysjunction); combined anomalies of gastrulation and primary neurulation and anomalies of secondary neurulation. Correlation with clinical and embryological data and common imaging findings provides an organized approach in their diagnosis.

Spinal dysraphism refers to the congenital abnormalities of the spine and spinal cord. Clinico-radiological classification of spinal dysraphism has been well established and widely followed. The objective of this article is to illustrate the common magnetic resonance imaging (MRI) findings of various spinal dysraphisms based on embryological events

Spinal dysraphism is an umbrella term that describes a number of conditions present at birth that affect the spine, spinal cord, or nerve roots.

• Spine: the bony structure also known as the spinal column. Made up of individual vertebrae (bones), the spine protects the spinal cord.
• Spinal cord: the bundle of nerves and other tissue that connects brain and body. Inside the spine, the spinal cord is also protected by a series of membranes (coverings). The spinal cord relays sensory information from the body to the brain, and movement instructions from the brain to the body.
• Nerve roots: nerves that branch off the spinal cord to reach the rest of the body.

All forms of spinal dysraphism result from an event very early in an embryo’s development. In about the third week of development, a sheet of cells called the neural plate folds up to form a structure called the neural tube. The top of the neural tube develops into the brain, and the rest of the neural tube develops into the spine and spinal cord. Spinal dysraphism results when a section of the neural tube that will become the spine and spinal cord does not close completely.

Types of spinal dysraphism include myelomeningocele (also known as spina bifida aperta or open spina bifida), spina bifida occulta, split cord malformation (diastematomyelia), spinal cord lipoma (lipomyelomeningocele), dermal sinus tract, tight filum terminale, and tethered spinal cord. A person with spinal dysraphism may have more than one type.

• Myelomeningocele, or spina bifida aperta: a condition in which the spinal cord and its membranes are not contained within the spinal column, but protrude into a sac outside the body
• Spina bifida occulta: a condition in which one or more vertebrae (bones of the spinal column) has a slight defect, but the spinal cord and its membranes are not affected
• Split cord malformation (diastematomyelia): a complex type of spinal dysraphism in which the spinal cord splits lengthwise into two distinct cords. Often, the split is caused by a thin segment of bone or cartilage that protrudes from the spinal column into the spinal cord space. Sometimes there is only one protective membrane or sleeve (the dura) around both parts of the spinal cord. Sometimes each part has its own dural sleeve.

• Spinal cord lipoma (lipomyelomeningocele): a condition in which an abnormal growth of fat attaches to the spinal cord, its membranes, and the space outside the spinal canal.   Dermal sinus tract : a channel in the skin that may reach all the way to the spinal cord. Dermal sinus tracts are often associated with tumors in the space around the spinal cord called dermoids or epidermoids. Benign (non-cancerous) tumors and cysts can be found along with any type of spinal dysraphism. Tumor types include lipoma (a fatty tumor), dermoid(a tumor containing tissue of hair, bone, or cartilage), and epidermoid(a tumor of skin layers). These tumors are not cancerous and will not spread. However, they may compress the spinal cord or
• tethered spinal cord.Tethered cord: a condition that may occur as a result of any spinal dysraphism, or as a result of other conditions (e.g. tumor, infection, or scar tissue formation). In this condition, the spinal cord is restricted at its base and cannot move freely in the spinal column. The resulting “stretch” on the spinal cord tissue can cause damage to the spinal cord leading to neurological problems (weakness, sensory loss), urological problems (incontinence), orthopedic problems (scoliosis and foot, ankle or leg deformities) and pain (see below). Accumulations of fluid in the spinal cord can also occur.

CLASSIFICATION-

Spinal dysraphism can be broadly divided into two different clinicoradiological entities ^8,9:

• open spinal dysraphism (formerly spina bifida aperta or cystica): occurs when the cord and its covering communicate with the outside; no skin or tissues cover the sac
  • myelomeningocele (98% of open spinal dysraphism)
  • myelocele
  • hemimyelomeningocele
  • hemimyelocele
• closed spinal dysraphism (formerly spina bifida occulta): occurs when the cord is covered by other normal mesenchymal elements
  • with subcutaneous mass
    • lipoma with dural defect
      • lipomyelomeningocele
      • lipomyelocele
    • terminal myelocystocele
    • meningocele
    • limited dorsal myeloschisis
  • without subcutaneous mass
    • posterior spina bifida (isolated defect of the posterior neural arch of vertebra)
    • intradural lipoma
    • filar lipoma
    • tight filum terminale
    • persistent terminal ventricle
    • disorders of midline notochordal integration
      • dorsal dermal sinus
      • dorsal enteric fistula
      • neurenteric cyst ^5,6
      • split cord malformations
        • diastematomyelia
        • diplomyelia
    • disorders of notochordal formation
      • caudal regression syndrome
        • Type 1
        • Type 2
      • segmental spinal dysgenesis

CAUSE AND RISK FACTOR-

The causes of spinal dysraphism are not yet completely understood. Genetic and environmental factors both seem to play a role.

The spinal cord arises very early in fetal development–in the first several weeks of gestation. Many forms of spinal dysraphism develop during this time. Robust maternal nutrition early in pregnancy, especially adequate levels of a vitamin called folate, seems to protect against some forms of spinal dysraphism.

SPINAL CORD DEVELOPMENT-

Spinal cord development can be summarized in three basic embryologic stages – gastrulation (2–3 weeks), primary neurulation (3-4 weeks) and secondary neurulation (5–6 weeks). The rostral spinal cord (to about the level of S2) is formed by primary neurulation and the caudal spinal cord (distal to S2 level) by secondary neurulation, also referred to as canalization and retrogressive differentiation.

Gastrulation-

Gastrulation is the process of conversion of bilaminar disc into a trilaminar disc initiated by primitive streak. Primitive node, a depression at the cranial end of streak, contains cells that are important for organizing the embryonic axes. Epiblast cells migrate toward and through the streak and node, detach and form two new layers ventral to the remaining epiblast. The first cells through the streak displace the original hypoblast to form endoderm, whereas cells migrating slightly later create a new middle layer, the mesoderm. Nonmigrating cells of epiblast constitute the ectoderm. Some cells migrate cranially in the midline to form the prechordal plate and notochord, which initiate the process of neurulation by inducing the formation of the neural plate from overlying ectoderm cells. Thus, neural plate is derived from ectoderm and forms in the central part of this upper layer. Remainder of the ectoderm surrounding the neural plate forms the epidermis.

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

PRIMARY NUTRITION-

Lateral borders of neural plate elevate into neural folds which later fuse in the midline to form the neural tube . The open regions of the neural tube called the anterior (cranial) and posterior (caudal) neuropores close by the zippering process. This neurulation process is called primary neurulation which is responsible for establishing brain and spinal cord regions down to the sacral levels (probably up to S2). On neural tube closure, overlying non-neural epidermal cells form the ectodermal layer of the skin. Normal neural tube closure occurs by day 25 to 27. Meanwhile, the neural tube separates from the overlying ectoderm, a process called dysjunction.

The neuroepithelial cells (neuroblasts) around the inner neural tube form the mantle layer, which produces the spinal cord gray matter. The outermost layer forms the marginal layer, which subsequently myelinates to produce the spinal cord white matter. The central neuroepithelial cells differentiate into ependymal cells along the central canal. Neural crest cells along each side of the neural tube form the dorsal root ganglia, autonomic ganglia, Schwann cells, leptomeninges and adrenal medulla.

SECONDARY NUTRITION-

The cord caudal to S2 level is formed by this process. Totipotent mesodermal cells called caudal cell mass or tail bud coalesce to form neural tube which then epithelialize, reorganize around a lumen and finally become continuous with the cranial part of the tube initially formed by primary neurulation. Part of the caudal cell mass undergoes both regression and differentiation (a process called retrogressive differentiation) to form filum terminale, terminal ventricle, tip of conus medullaris, and most of the sacrum, coccyx and coccygeal medullary vestige. By the third gestational month, spinal cord extends the entire length of the developing spinal column. Rapid elongation of the vertebral column and dura relative to the cord produces the apparent ascent of the cord during the remainder of the gestation and the conus is at the adult level soon after birth.

Clinico-radiologically, spinal dysraphism is classified into two categories. The first category is spinal dysraphism with back mass that is not covered by skin, i.e. open dysraphism. The second is spinal dysraphism with skin-covered back mass, i.e. closed dysraphism, which can be further subcategorized on the basis of the presence or absence of a subcutaneous mass.

Anomalies of Gastrulation-

Failure of notochord formation causes complex dysraphic states such as caudal regression syndrome and segmental spinal dysgenesis. Incorrect notochordal induction leads to the incomplete splitting of the neural plate from the notochord, producing the split notochord syndromes (neurenteric cyst and diastematomyelia).

Failure of notochord formation causes complex dysraphic states such as caudal regression syndrome and segmental spinal dysgenesis. Incorrect notochordal induction leads to the incomplete splitting of the neural plate from the notochord, producing the split notochord syndromes (neurenteric cyst and diastematomyelia).

Anomalies of notochord formation

Caudal regression syndrome

Caudal regression syndrome (CRS) is a complex dysraphic state with aberrations in gastrulation, secondary as well as primary neurulation. Most cases are sporadic, although a dominantly inherited defect in the HLXB9 gene has been described. Mothers of 15–20% of these infants are diabetic, and the offspring of 1% diabetic mothers are afflicted. Associations with other caudal spinal segment anomalies such as vertebral segmentation and formation anomalies and split cord malformations are noted.

Two types are described. Type 1 features a foreshortened terminal vertebral column, high-lying wedge-shaped conus termination and more severe associated visceral and orthopedic anomalies. Type 2 is less severe and has a low-lying tethered spinal cord with milder associated malformations In general, the higher the cord termination, the more severe is the sacral anomalies. The most severe CRS presentations are lumbosacral agenesis in which the spine terminates at the lower thoracic level and there is severe sacral dysgenesis with fused lower extremities in a “mermaid” configuration (sirenomyelia)

Segmental spinal dysgenesis (SSD) is a very rare dysraphic anomaly characterized by segmental thoracolumbar or lumbar vertebral and spinal cord dysgenesis or agenesis. Congenital thoracic or lumbar kyphosis is characteristic, with a palpable dorsal bone spur located at the gibbous apex. The upper spinal cord is normal, however, the cord segment below the dysgenetic segment is bulky, thickened and low-lying. The spinal canal proximal and distal to the dysgenetic level is of normal caliberSegmental spinal dysgenesis (SSD) is a very rare dysraphic anomaly characterized by segmental thoracolumbar or lumbar vertebral and spinal cord dysgenesis or agenesis. Congenital thoracic or lumbar kyphosis is characteristic, with a palpable dorsal bone spur located at the gibbous apex. The upper spinal cord is normal, however, the cord segment below the dysgenetic segment is bulky, thickened and low-lying. The spinal canal proximal and distal to the dysgenetic level is of normal caliberSegmental spinal dysgenesis (SSD) is a very rare dysraphic anomaly characterized by segmental thoracolumbar or lumbar vertebral and spinal cord dysgenesis or agenesis. Congenital thoracic or lumbar kyphosis is characteristic, with a palpable dorsal bone spur located at the gibbous apex.

Neurenteric cyst and dorsal-enteric spinal anomalies

Neurenteric cyst (NEC) is a complex dysraphic state and consists of an intraspinal cyst lined by enteric mucosa. It is most common in thoracic spine followed by cervical spine. They arise from an abnormal connection between primitive endoderm and ectoderm that persists beyond the third embryonic week. Normally, the notochord separates ventral endoderm (foregut) and dorsal ectoderm (skin, spinal cord) during embryogenesis, in an NEC, a separation failure “splits” the notochord and hinders the development of mesoderm, which traps a small piece of primitive gut within the developing spinal canal. This gut remnant may become isolated forming a cyst or it may maintain connections with gut or skin (or both); this produces the spectrum of fistulas and sinuses that constitute the spectrum of dorsal-enteric spinal anomalies.

The upper spinal cord is normal, however, the cord segment below the dysgenetic segment is bulky, thickened and low-lying. The spinal canal proximal and distal to the dysgenetic level is of normal caliber.

Abnormalities of Primary Neurulation

Premature dysjunction

If dysjunction occurs prematurely, perineural mesenchyme is interposed between neural tube and ectoderm, which may differentiate into fat and prevent complete neural tube closure. It leads to the lipomatous malformation spectrum of lipomyelocele, lipomyelomeningocele and spinal lipomas.

Lipomyelocele (LMC), b) lipomyelomeningocele (LMMC)

The main differentiating feature between a LMC and LMMC is the position of the placode–lipoma interface.With an LMC, the placode–lipoma interface lies within the spinal canal. With an LMMC, the placode–lipoma interface lies outside of the spinal canal due to expansion of the sub-arachnoid space and In both cases, syringomyelia is a commonly associated finding. LMC and LMMC account for 20–56% of occult spinal dysraphism and 20% of skin-covered lumbosacral masses. An important imaging point is that the neural placode is frequently rotated; this foreshortens the roots on one side, predisposing them to stretch injury, and lengthens the roots on the other side, rotating them into the surgeon’s field of view and making them more prone to injury.

The spinal lipoma

The spinal lipoma is a simple dysraphic state and is subdivided into intradural and terminal (filar) lipomas. An intradural lipoma refers to a lipoma located along the dorsal midline that is contained within the dural sac. No open spinal dysraphism is present. They are most commonly lumbosacral in location. Fibrolipomatous thickening of the filum terminale is referred to as a filar lipoma. Filar lipomas can be considered a normal variant if there is no clinical evidence of tethered-cord syndrom.

Nondysjunction

Nondysjunction results from failure of dissociation of neural tube from adjacent cutaneous tissue. If dysjunction fails to occur, an ectodermal–neuroectodermal tract forms that prevents mesenchymal migration. Nondysjunction results in open neural tube defect spectrum of dorsal dermal sinus, myelomeningocele, and myeloceles.

Dorsal dermal sinus

The simplest of these is the dorsal dermal sinus connecting skin dimple to the dural sac, conus, or central spinal cord canal. The most common dermal sinus tract (DST) location is in the lumbosacral spine, followed by the occiput. In all dermal sinus cases, there is some degree of focal dysraphism, which may be as subtle as a bifid spinous process. The true congenital dorsal DST usually has an atypical dimple at the ostium that is large (>5 mm), often asymmetric, and remote (>2.5 cm) from the anus A. These features help distinguish the dermal sinus from its clinically asymptomatic mimic, simple coccygeal dimple. The sinus tract/cord is epithelial-cell lined and may or may not be canalized. When patent, it exposes the patient to an elevated risk of meningitis. It is critical to look for this anomaly in all patients with atypical skin dimples, cutaneous back lesions or lipomas. Moreover, 30–50% of DSTs may have an associated dermoid or epidermoid cyst.

Myelomeningocele and myelocele

Myelomeningoceles and myeloceles are caused by defective closure of the primary neural tube and are clinically characterized by exposure of the neural placode through a midline skin defect on the back, and hence, classified under open dysraphic states. Myelomeningoceles account for more than 98% of open spinal dysraphisms. Myeloceles are rare. It is important to note that preoperative imaging of myelomeningocele is usually not done because of the risk of infection. Nevertheless, the main differentiating imaging feature between a myelomeningocele and myelocele is the position of the neural placode relative to the skin surface. The neural placode protrudes above the skin surface with a myelomeningocele and is flush with the skin surface with a myelocele. Myelomeningocele is almost always seen in the context of a Chiari 2 malformation.

Combined Anomalies of Gastrulation and Primary Neurulation

Hemimyelomeningocele and hemimyelocele

Hemimyelomeningoceles and hemimyeloceles can also occur but are extremely rare. These conditions occur when a myelomeningocele or myelocele is associated with diastematomyelia (cord splitting) and one hemicord fails to neurulate.

Anomalies of Secondary Neurulation/anomalies of the Caudal Cell Mass

Failure of expected secondary neurulation leads to conditions such as abnormally long spinal cord, tethered cord syndrome, persisting terminal ventricle, terminal myelocystocele, lipoma of filum terminale and intrasacral – anterior sacral meningocele. It is also implicated in pathogenesis of caudal regression syndrome and segmental spinal dysgenesis.

Persistent terminal ventricle/fifth ventricle

By day 48, a transient ventriculus terminalis appears in the future conus. According to Coleman et al., evidence of a fifth ventricle not accompanied by other pathologies is a frequent finding that does not have pathological significance during the first 5 years of life.

Key imaging features include location immediately above filum terminale and lack of contrast enhancement, which differentiates this entity from other cystic lesions of the conus medullaris.

Tethered cord syndrome

Tethered cord syndrome (TCS) patients most likely present during periods of rapid somatic growth. It manifests clinically as gait spasticity, low back and leg pain that is worse in the morning, lower extremity sensory abnormalities, and/or bladder difficulties. On imaging, TCS strictly refers to patients with a low-lying cord and thickened filum [>1.5 mm] .

Intrasacral – anterior sacral meningocele

The term “intrasacral meningocele” is used to denote a sac lined by arachnoid which lies within an enlarged sacral spinal canal and is attached to the caudal termination of the dural sac by a pedicle that usually permits cerebrospinal fluid (CSF) flow from the tip of the subarachnoid space into the meningocele. Consistent with the possible congenital origin, intrasacral meningocele may occur in association with other anomalies such as sacral vertebral anomalies, diastematomyelia or TCS

Anterior meningoceles are usually presacral in location. It has a large anterior meningocele outpouching that traverses an enlarged sacral foramen and produces a presacral cystic mass. Most ASMs are sporadic but a minority show an inherited predisposition within the Currarino triad or in syndromes that feature dural dysplasia, such as neurofibromatosis type 1 (NF1) and Marfan syndrome.

Terminal myelocystocele

Herniation of a large terminal syrinx (syringocele) into a posterior meningocele through a posterior spinal defect is referred to as a terminal myelocystocele. The terminal syrinx component communicates with the central canal, and the meningocele component communicates with the subarachnoid space. The terminal syrinx and meningocele components do not usually communicate with each other.

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

INTRODUCTION-

This study explored premorbid, neurocognitive, behavioral, and familial factors in preschoolers, ages 3–6, who experienced a mild to moderate traumatic brain injury (TBI). Twenty-nine children with TBI, 33 children with mild to moderate injuries to other body regions, and 34 non-injured children participated in the study. Neuropsychological assessments and behavioral measures were administered at the time of hospitalization and 6 months later. In comparison to the non-injury children, preschool-aged children with TBI had higher rates of premorbid behavior difficulties, lower premorbid cognitive functioning, and poorer development of pre-academic skills. In addition, parents of children with TBI reported greater situational issues and life stressors than parents of children in the non-injured group. Some neurocognitive recovery was evident in the TBI group, but no differences were recognized in behavioral and family measures at the 6-month follow-up. This study emphasizes the relative effects of premorbid characteristics in later practice of preschool children who sustain TBI.

The purpose of this study was to compare child, hospital course, and discharge characteristics by admitting unit, injury type, head Abbreviated Injury Scale (AIS), and Glasgow Coma Scale (GCS), and test congruence of AIS and GCS categories. Chart data were collected from seven hospitals on 183 preschool children with head injury (90 admitted to PICU, 93 to general care unit). Injury events included falls (n = 89, 49%), hit by car (n = 35, 19%), motor vehicle crashes (n = 26, 14%), bicycle crashes (n = 12, 7%), and blunt traumas (n = 21, 11%). Most children (68%) had head injuries only, 20% had other fractures, 5% had organ damage, and 7% had all three. Injury severity was measured by head AIS and GCS scores. Treatments and procedures included tubes/lines, blood/blood products, and medications. Children with head injuries only had fewer hospital days, less severe head injuries, and near normal GCS scores. They were less likely to have tubes/lines and medications. Children were discharged with medications (61%) and medical equipment (14%). Five children were discharged to long-term care facilities, and five were discharged to rehabilitation facilities. Concordance of head AIS and GCS categories occurred for only 50 (28%) children. Although the GCS is the gold standard for identifying changes in neurological status, it was not as helpful in representing hospital care. Head AIS injury categories clustered children in more homogeneous groups and better represented hospital care. Head AIS categories are better indicators of injury severity and care provided than GCS. Head injury AIS score may be an important addition to GCS for guiding care.

Traumatic brain injury (TBI), sometimes referred to as a silent epidemic, effects thousands of people each year. Incidence of pediatric TBI is 220 per 100,000. Head trauma is placed as the major cause of death in children, with a mortality rate of 10 per 100,000 children (Annegers, 1983). This mortality rate alone, although concerning, does not fully describe the impact of TBI. Approximately 100,000–170,000 children are hospitalized each year with a TBI, and six times that visit the emergency room (Eiben et al., 1984; Kraus, Fife, Cox, Ramstein, & Conroy, 1986). In their 1974 study, Kalsbeck, McLaurin, Harris, & Miller (1980) reported that the direct and indirect costs of pediatric TBI were as much as 348 million dollars per year. These statistics indicate that TBI is a major public health problem, and a significant health-related financial burden (Gotschall, 1993).

While there is substantial literature on the effects of mild to moderate TBI on school-aged children, relatively little is known about mild to moderate TBI in preschool-aged children. Preschool TBI is a complex condition, which may have different outcomes depending upon the premorbid status of the child, the functional status of the family, and the severity of the injury. Research into the effects of TBI in preschoolers may allow us to understand this common childhood disorder better. To date, the limited literature on the preschool age group has focused primarily on the outcomes of severe TBI, so studies on mild and moderate TBI are greatly needed.

Research into preschool TBI is also important because it promises to further our understanding of the developmental variability of TBI throughout childhood, and perhaps expand our knowledge of the complex interplay between age of injury, severity of injury, and mechanism of injury in acquired childhood brain injury. Both animal and human studies of brain injury suggest that the age at which injury was sustained is a major contributor to eventual outcome. In general, evidence does not support the notion that the young brain is less vulnerable to insult or recovers better than the mature brain. We do not know, however, whether this is true of all ages, etiologies, or severity levels of traumatic injuries. In a review of research on age factors in TBI, Fletcher and Levin (1988) found evidence for greater compromise in children less than 6 years of age. However, the worse outcome in the younger sample may have been colored by a high rate of TBI from abuse. It is now known that abused children may suffer more severe injuries, they may differ from non-abused children prior to the injury, and they tend to have a worse general outcome from traumatic brain injury due to pathophysiological factors unique to abuse (Goldstein, Kelly, Bruton, & Cox, 1993; Michaud, Rivara, Grady, & Reay, 1992; Trickett & Aber, 1991). When a sub-sample of physically abused children was removed from analyses, younger and older children with severe injury had similar outcomes (Kriel, Krach, & Panser, 1989). There are other studies not including abuse as a confound, which suggest somewhat worse outcome in younger children equated for severity of injury with older children (Ewing-Cobbs, Levin, Eisenberg, & Fletcher, 1987; Gulbrandsen, 1984; Levin, Eisenberg, Wigg, & Kobayashi, 1982), especially for preschoolers (Michaud, Rivara, Jaffe, Fay, & Dailey, 1993; Wrightson, McGinn, & Gronwall, 1995).

Wrightson et al. (1995) concluded that preschoolers with severe traumatic brain injury might fare far worse than older children. This may, in part, be due to the latency in symptom manifestation with the deficit taking years to become evident. These late cognitive effects are known as patients “growing into their deficits” (Grattan & Eslinger, 1991; Kolb, 1995). In a retrospective analysis of school-aged children, Michaud et al. (1993) reported that children in special education classes had a higher incidence of preschool head injury than children in regular classes. Similarly, Gronwall, Wrightson, and McGinn (1997) found that significantly more children who had a history of TBI in the preschool years needed special assistance with reading than children who had no injury prior to beginning school. The first study certainly suggests that younger children with severe injury fare more poorly than older children. The latter two suggest that preschoolers with milder injury fare more poorly as well, but these studies are retrospective in nature, inferring TBI sequelae years after the event. One case study suggested that preschoolers might be vulnerable to mild head injury and show delayed effects. PET and neuropsychological testing documented hypometabolism in both temporal lobes, and verbal and visual memory deficits, respectively, in a young child who sustained whiplash injury in a motor vehicle accident. Staring spells, brief confusional episodes, and emotional outbursts were noted 2 years after injury, and epileptiform activity was documented on EEG 4 years post-trauma (Roberts, Manshadi, Bushnell, & Hines, 1995).

The age at which the child is injured may also affect the manifestation of cognitive dysfunction. There is increasing evidence that skills in a rapid state of development at injury may be more vulnerable to the effects of severe TBI. Preschoolers are likely to demonstrate compromise in motor and expressive language skills (Ewing-Cobbs, Miner, Fletcher, & Levin, 1989) and school-aged children may be more compromised in reading (Shaffer, Chadwick, & Rutter, 1975) and written language (Ewing-Cobbs et al., 1987). The results of one retrospective study suggested that preschoolers had greater impairment in reading (Gronwall et al., 1997).

A prospective study of preschoolers with mild to moderate TBI can help assess whether recovery patterns parallel that of older children and adults, as reported in the literature. Initial cognitive deficit is common in older children, but there is little evidence of sustained neurocognitive or learning deficits in the majority of children (Asarnow et al., 1995; Bawden, Knights, & Winogren, 1985; Bijur & Haslum, 1995; Chadwick, Rutter, Brown, Shaffer, & Traub, 1981a; Gulbrandsen, 1984, Levin et al., 1988). Again, some of the research suggests that preschoolers may be especially vulnerable even to mild TBI.

Rutter, Chadwick, Shaffer, & Brown (1980) have further suggested that many of the deficits evident in children with a history of TBI predated the injury. Studies have documented pre-existing developmental difficulties and specific learning problems (Klonoff & Paris, 1974), language problems (Mahoney et al., 1983), and lower academic achievement (Chadwick, Rutter, Brown, Shaffer, & Taub, 1981b) in preschoolers who sustain TBI. Demographic risk factors for all childhood injury include poverty, single-family households, and congested living conditions. Psychiatric histories, drug/alcohol histories, and physical illness are found more frequently in the parents of injured children. Unsupervised play is also reported more frequently, which may be directly related to incidence of injury (Chadwick et al., 1981b; Klonoff & Paris, 1974). It is possible that pre-existing cognitive problems will also affect incidence of injury due to the child’s inability to evaluate risks and dangers.

Many studies also suggest the child with traumatic brain injury is more likely to have a history of behavioral disorder (Bijur & Haslum, 1995; Brown, Chadwick, Shaffer, Rutter, & Traub, 1981; Chadwick et al., 1981b; Klonoff, 1971; Klonoff & Paris, 1974). In a sample of 100 pediatric patients suffering traumatic brain injury, Arffa (1995) found that 55% had a history of either school learning difficulties, behavioral problems, or emotional disturbance. Child behavioral characteristics associated with high traumatic brain injury rates include impulsivity, aggression, and attention seeking behavior. These characteristics might also be seen as proximal causes of injury. Behavioral factors in the toddler are secondary to home environment in the injury equation (Matheny, 1987). A previous history of traumatic brain injury is also associated with an increased risk of further traumatic brain injury (Annegers, 1983). Multiple TBI’s are strongly related to socioeconomic factors and behavioral characteristics such as hyperactivity and aggression (Bijur & Haslum, 1995).

Some studies have found an interaction between new behavioral disturbance and TBI severity, but variation among studies occur depending on the criteria used to describe behavior problems or change (Brink, Imbus, & Woo-Sam, 1980; Fletcher, Ewing-Cobbs, Miner, Levin, & Eisenberg, 1990; Rivara et al., 1994). In the studies by Rutter and colleagues, the rate of new psychiatric disorder was three times more common in severely head injured children than in orthopedic injury controls (Brown et al., 1981; Rutter, Chadwick, & Shaffer, 1983). Behavioral disposition may actually worsen over time in severe injury (Fletcher, Ewing-Cobbs, Francis, & Levin, 1995). A severity threshold was proposed as psychiatric disorder became much more likely in very severe injury (post-traumatic amnesia for more than 22 days) than in severe (7–21 days of post-traumatic amnesia) or mild injuries. Threshold effects noted in other studies (Levin & Eisenberg, 1979) were lower than that of Brown and Rutter. No significant difference in rate of new psychiatric disorder was observed in children with mild injuries when contrasted with orthopedic control groups (Brown et al., 1981, Fletcher et al., 1990, Rutter et al., 1983). Pre-injury behavior was found to be related to behavioral outcome in Rutter’s studies. Over one-half with a doubtful disorder developed a definable disorder and all had symptoms. A study by Rivara et al. (1993) yielded similar findings, reporting child behavior ratings obtained 1 year after TBI correlated with pre-injury ratings of child behavior.

Family functioning may be an important mediator of behavioral outcome in children with TBI, perhaps more important than neurocognitive function. Brown et al. (1981) found that children from problematic family backgrounds also were at high risk for developing new psychiatric disorders following the injury. Rivara et al. (1992) found that family functioning interacted with premorbid child characteristics. A deterioration of family functioning for children with severe TBI relative to children with mild or moderate TBI was also evident. Taylor et al. (1995) emphasized a link between child behavior problems and family stress, negative life events, and parental psychological symptoms. Perrott, Taylor, & Mantes (1991) proposed that family dysfunction may have adverse effects on subsequent child behavior and adaptation in spite of continuing cognitive recovery.

The present study was designed as a comprehensive exploration of the premorbid states of preschool-aged children with TBI, the immediate cognitive effects of TBI, and the post-acute cognitive and behavioral outcomes of TBI.

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

Materials and Methods-

Setting and Procedure

Hospital records of 183 preschool children (ages 36 through 83 months) who suffered a head injury were reviewed after parental consent. Children were hospitalized in one of seven tertiary care centers, including three free-standing children’s hospitals. Admission to the pediatric intensive care unit (PICU) versus a general care unit (GCU) was decided by the admitting physicians (not involved in the study) and hospital policy. Institutional Review Board approvals were obtained from the appropriate universities and hospitals.

For this research, head injury was defined as an injury event where a blow to the head was probable with at least one physical finding suggesting head trauma, including symptoms of head injury in children: loss of consciousness no matter how brief, emesis, drowsiness, seizures, neurological deficits, cerebrospinal fluid or bloody discharge from the ears or nose, or a positive CT scan or skull X-ray. To be eligible, the injured child was a) free from chronic illnesses other than asthma, b) not previously hospitalized other than at birth, and c) without severe pre-existing cognitive deficits. For purposes of the larger study, children had to be living with at least one biological or adoptive parent before the injury and expected to survive. Parents had to understand spoken English. Exclusion criteria necessary for the larger study were a) injury suspected to be due to child abuse, b) child meeting or being evaluated with brain death criteria, c) parent(s) hospitalized concurrently with major injury, or d) death of parent(s) in the injury event.

For this research, head injury was defined as an injury event where a blow to the head was probable with at least one physical finding suggesting head trauma, including symptoms of head injury in children: loss of consciousness no matter how brief, emesis, drowsiness, seizures, neurological deficits, cerebrospinal fluid or bloody discharge from the ears or nose, or a positive CT scan or skull X-ray. To be eligible, the injured child was a) free from chronic illnesses other than asthma, b) not previously hospitalized other than at birth, and c) without severe pre-existing cognitive deficits. For purposes of the larger study, children had to be living with at least one biological or adoptive parent before the injury and expected to survive. Parents had to understand spoken English. Exclusion criteria necessary for the larger study were a) injury suspected to be due to child abuse, b) child meeting or being evaluated with brain death criteria, c) parent(s) hospitalized concurrently with major injury, or d) death of parent(s) in the injury event.

Instruments

Injury severity was measured through hospital record review with the Abbreviated Injury Scale (AIS) and the Glasgow Coma Scale (GCS). Severity of the anatomical injuries for the AIS was determined with reports of clinically indicated procedures (X-ray, CT, magnetic resonance imaging [MRI], laboratory, operative) and chart notes recorded at the time of care by emergency room staff, emergency medical service providers (when available), and admitting physicians and nurses. Most GCS scores were recorded in the chart as part of the clinical care.

The AIS classifies severity of individual anatomical injuries by body regions, and therefore, does not change over time. Severity of injury in six body regions (head/neck, face, chest, abdomen, extremities/pelvic girdle, and external) is scored from one to six. The Injury Severity Scale (ISS) total score is calculated by summing the squares of the highest AIS code in the three body regions with the most severe injury. Severity scores for the AIS for a specific body region and the total ISS score are categorized as minor/mild, moderate, serious, severe, critical, and major/grave (AAAM, 1990). Children with “major/grave” injuries rarely survive, making them ineligible for the larger study. The severe and critical categories were combined because of the small number in each category. For this analysis, children’s head AIS scores were used to characterize the severity of head injury from mild to severe/critical. Three children’s head injuries were not scored because of lack of sufficient specific information in the chart to make a determination.

Results

2.1. Behavioral measures: premorbid estimates

2.1.1. Parenting Stress Index (PSI)

An analysis of variance (ANOVA) showed a significant difference between groups on the Life Stress Scale (F(2,86) = 4.2, p < .05), and Tukey’s post hoc analysis indicated that parents of TBI children reported significantly more stress than the children in the OI group (p < .05) and the NC group (p < .001). An ANOVA showed a significant difference between groups on the Defensive Responding Scale (F(2,86) = 4.2, p < .05), with the parents in the TBI group having a significantly higher rate of defensive responding than the parents in the NC group, suggesting that parents of TBI children may have underreported symptoms. Since analysis of the Defensive Responding Scale of the PSI indicated the possibility of parental underreporting of symptoms, correlations between scores on the Defensive Responding Scale and scores on all parent report questionnaires were examined. Significant correlations were followed by analyses of covariance to adjust statistically for between-group differences in defensive responding.

A multivariate analysis of covariance (MANCOVA), using the Defensive Responding Scale as a covariate, identified a significant covariate and group effect for the overall Child Domain Scale (F = (2,87) = 25.4, p < .001, r = .69; F = (2,86) = 7.8, p < .001) and Total Stress Scale (F = (2,87) = 53.8, p < .001, r = .63; F = (2,86) = 5.9, p < .001), but not the overall Parent Domain Scale. In addition, there were significant covariate and group effects for the Child Domain subtests of distractibility/hyperactivity (F = (2,87) = 16.7, p < .001, r = .44; F = (2,86) = 5.1, p < .005), adaptability (F = (2,87) = 18.7, p < .001, r = .48; F = (2,86) = 6.6, p < .005), demandingness (F = (2,87) = 21.1, p < .001, r = .51; F = (2,86) = 9.2, p < .001), and acceptibility (F = (2,87) = 22.8, p < .001, r = .48; F = (2,86) = 3.4, p < .05), as well as on the Parent domain subtests of Competence (F = (2,87) = 25.3, p < .001, r = .53; F = (2,86) = 8.3, p < .001) and Health (F = (2,87) = 37.6, p < .001, r = .59; F = (2,86) = 3.9, p < .05). Bonferroni post hoc contrasts revealed that children in the TBI group scored significantly higher than children in the NC group on distractibility/hyperactivity, adaptability, and acceptability. Children in the TBI group and OI group were found to be more demanding than children in the NC group. Parents from the NC group appeared to feel more confident in their parenting than parents in the TBI group and OI group. Parents from the OI group reported significantly better health than parents from the TBI group. displays the means, standard deviations, and p-values.

Table 2. MANCOVA group mean summary table on the PSI: acute testing

PSI scales	Group	p
	TBI	Other injury	Non-injury
	M	M	M
Total stress	35.44	38.61	30.65	.004**
Child domain	50.08	45.14	33.44	.001**
Parent domain	29.28	33.43	33.62	.262
Child domain subscales
Adaptability	57.48	44.18	39.88	.002**
Acceptability	47.36	44.25	39.26	.038*
Demandingness	54.04	51.54	35.35	.000***
Mood	59.48	53.61	53.50	.183
Distractibility/hyperactivity	47.00	40.43	32.03	.008**
Reinforces parent	52.12	49.36	50.65	.466
Parent domain subscales
Depression	28.56	36.07	34.50	.215
Attachment	44.04	40.39	35.97	.219
Role restriction	28.68	32.25	45.50	.635
Competence	33.72	35.11	22.12	.001**
Isolation	41.92	43.50	52.91	.644
Spouse	43.28	43.07	46.76	.468
Health	49.32	36.14	50.56	.024*
Defensive responding	0.44	0.32	0.12	.018*
Life stress	67.48	43.59	27.26	.000***

Note: means were adjusted using defensive responding as a covariate. ^*p < .05, ^**p < .01, ^***p < .001

The importance of early childhood experiences for brain development

Children are born ready to learn, and have many skills to learn over many years. They depend on parents, family members, and other caregivers as their first teachers to develop the right skills to become independent and lead healthy and successful lives. How the brain grows is strongly affected by the child’s experiences with other people and the world. Nurturing care for the mind is critical for brain growth. Children grow and learn best in a safe environment where they are protected from neglect and from extreme or chronic stressexternal icon with plenty of opportunities to play and explore.

Parents and other caregivers can support healthy brain growth by speaking to, playing with, and caring for their child. Children learn best when parents take turns when talking and playing, and build on their child’s skills and interests. Nurturing a child by understanding their needs and responding sensitively helps to protect children’s brains from stress. Speaking with children and exposing them to books, stories, and songs helps strengthen children’s language and communication, which puts them on a path towards learning and succeeding in school.

Exposure to stress and trauma can have long-term negative consequences for the child’s brain, whereas talking, reading, and playing can stimulate brain growth. Ensuring that parents, caregivers, and early childhood care providers have the resources and skills to provide safe, stable, nurturing, and stimulating care is an important public health goal.

When children are at risk, tracking children’s development and making sure they reach developmental milestones can help ensure that any problems are detected early and children can receive the intervention they may need.

Learn more about supporting early childhood experiences:

• Tracking developmental milestones
• Preventing abuse and neglect
• Positive parenting tips
• Healthy childcareexternal icon

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

A healthy start for the brain

To learn and grow appropriately, a baby’s brain has to be healthy and protected from diseases and other risks. Promoting the development of a healthy brain can start even before pregnancy. For example, a healthy diet and the right nutrients like sufficient folic acid will promote a healthy pregnancy and a healthy nervous system in the growing baby. Vaccinations can protect pregnant women from infections that can harm the brain of the unborn baby.

During pregnancy, the brain can be affected by many types of risks, such as by infectious diseases like Cytomegalovirus  or Zika virus, by exposure to toxins, including from smoking or alcohol, or when pregnant mothers experience stress, trauma, or mental health conditions like depression. Regular health care during pregnancy can help prevent complications, including premature birth, which can affect the baby’s brain. Newborn screening can detect conditions that are potentially dangerous to the child’s brain, like phenylketonuria (PKU). external icon

Healthy brain growth in infancy continues to depend on the right care and nutrition. Because children’s brains are still growing, they are especially vulnerable to traumatic head injuries, infections, or toxins, such as lead. Childhood vaccines, such as the measles vaccine, can protect children from dangerous complications like swelling of the brain. Ensuring that parents and caregivers have access to healthy foods and places to live and play that are healthy and safe for their child can help them provide more nurturing care.

Learn more about the recommended care:

• Before pregnancy
• During pregnancy
• Around birth
• During infancy
• During early childhood

Initiation of physical, occupational, and speech therapy in children with traumatic brain injury

Abstract

Objectives: (1) To determine factors associated with physical therapy (PT) or occupational therapy (OT) evaluation and speech or swallow therapy evaluation in hospitalized children with traumatic brain injury (TBI); (2) to describe when during the hospital stay the initial therapy evaluations typically occur; and (3) to quantify any between-hospital variation in therapy evaluation.

Design: Retrospective cohort study.

Setting: Children’s hospitals participating in the Pediatric Health Information System database (January 2001-June 2011).

Participants: Children (age <18y) with TBI (N=21,399) who were admitted to the intensive care unit and survived to hospital discharge.

Interventions: Not applicable.

Main outcome measures: PT or OT evaluation and speech or swallow therapy evaluation. A propensity score was calculated to allow comparison of expected with observed rates of therapy evaluations by the hospital.

Results: The median hospital length of stay was 5 days (interquartile range, 3-10d). Overall, 8748 (41%) of 21,399 children received either a PT or OT evaluation, and 5490 (26%) out of 21,399 children received either a speech or swallow evaluation. Older children and those with higher energy injury mechanisms, more severe injuries, extremity fractures, more treatment with neuromuscular blocking agents or pentobarbital, and admission to a hospital with an American College of Surgeons Level I pediatric trauma designation were more likely to receive therapy evaluations. The median time until the first therapy evaluation was 5 (PT or OT) and 7 days (speech or swallow). Expected hospital evaluation rates were 25% to 54% (PT or OT) and 16% to 35% (speech or swallow), while observed hospital evaluation rates were 11% to 74% (PT or OT) and 4% to 55% (speech or swallow).

Conclusions: There is wide between-hospital variation in provision of rehabilitation therapies for children with TBI. Evidence-based criteria for initiation of routine therapy evaluations after TBI are needed.

Abstract

Objective: To describe the use of occupational therapy (OT), physical therapy (PT), and speech therapy (ST) treatment activities throughout the acute rehabilitation stay of patients with traumatic brain injury.

Design: Multisite prospective observational cohort study.

Setting: Inpatient rehabilitation settings.

Participants: Patients (N=2130) admitted for initial acute rehabilitation after traumatic brain injury. Patients were categorized on the basis of admission FIM cognitive scores, resulting in 5 fairly homogeneous cognitive groups.

Interventions: Not applicable.

Main outcome measures: Percentage of patients engaged in specific activities and mean time patients engaged in these activities for each 10-hour block of time for OT, PT, and ST combined.

Results: Therapy activities in OT, PT, and ST across all 5 cognitive groups had a primary focus on basic activities. Although advanced activities occurred in each discipline and within each cognitive group, these advanced activities occurred with fewer patients and usually only toward the end of the rehabilitation stay.

Conclusions: The pattern of activities engaged in was both similar to and different from patterns seen in previous practice-based evidence studies with different rehabilitation diagnostic groups.

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

INTRODUCTION-

A premature birth is a birth that takes place more than three weeks before the baby’s estimated due date. In other words, a premature birth is one that occurs before the start of the 37th week of pregnancy.

Premature babies, especially those born very early, often have complicated medical problems. Typically, complications of prematurity vary. But the earlier your baby is born, the higher the risk of complications.

Depending on how early a baby is born, he or she may be:

• Late preterm, born between 34 and 36 completed weeks of pregnancy
• Moderately preterm, born between 32 and 34 weeks of pregnancy
• Very preterm, born at less than 32 weeks of pregnancy
• Extremely preterm, born at or before 25 weeks of pregnancy

Most premature births occur in the late preterm stage.

A baby born before 37 weeks of pregnancy is considered premature or born too early. Other terms used for prematurity are preterm and preemie. The number of premature births in the U.S increased from 1990 to 2006 and has since been declining. Twins and other multiples are more likely to be premature than single birth babies. 

Many premature babies weigh less than 5 pounds, 8 ounces (2,500 grams). They may be called low birth weight. Even older, heavier preemies are still at risk for some problems. 

A typical pregnancy lasts about 40 weeks, yet some babies arrive sooner. A premature birth is a birth that takes place before the 37th week of pregnancy.

While some premature babies have serious medical complications or long-term health problems, many also go on to live normal healthy lives. With modern medicine and new technologies, babies are often able to survive when born earlier during the pregnancy. The dedicated staff in hospital neonatal intensive care units (NICU) and advancements in neonatal care have also improved outcomes. These advancements include:

• family integrated care programs
• nutrition management
• skin-to-skin contact with premature babies
• efforts to reduce the number of infections in premature babies

While outcomes have improved for premature babies, complications can still occur. The following complications can affect preterm babies in the first weeks after birth.

CAUSES-

Premature birth may have a number of causes. About 4 out of 5 premature births are because of  issues that directly cause early labor and birth, such as those listed below. Other problems can make the mother or baby sick and need early delivery. Sometimes the exact cause for a premature birth is unknown. This can be true even though the mother may have done everything right during the pregnancy. 

Four things that may cause premature labor are:

• Being pregnant with more than one baby
• Bleeding or other problems with the uterus
• Stress
• Infection in the uterus or elsewhere in the body

SYMPTOM-

Your baby may have very mild symptoms of premature birth, or may have more-obvious complications.

Some signs of prematurity include the following:

• Small size, with a disproportionately large head
• Sharper looking, less rounded features than a full-term baby’s features, due to a lack of fat stores
• Fine hair (lanugo) covering much of the body
• Low body temperature, especially immediately after birth in the delivery room, due to a lack of stored body fat
• Labored breathing or respiratory distress
• Lack of reflexes for sucking and swallowing, leading to feeding difficulties

The following tables show the median birth weight, length and head circumference of premature babies at different gestational ages for each sex.

Weight, length and head circumference by gestational age for boys
Gestational age	Weight	Length	Head circumference
40 weeks	7 lbs., 15 oz. (3.6 kg)	20 in. (51 cm)	13.8 in. (35 cm)
35 weeks	5 lbs., 8 oz. (2.5 kg)	18.1 in. (46 cm)	12.6 in. (32 cm)
32 weeks	3 lbs., 15.5 oz. (1.8 kg)	16.5 in. (42 cm)	11.6 in. (29.5 cm)
28 weeks	2 lbs., 6.8 oz. (1.1 kg)	14.4 in. (36.5 cm)	10.2 in. (26 cm)
24 weeks	1 lb., 6.9 oz. (0.65 kg)	12.2 in. (31 cm)	8.7 in. (22 cm)

Weight, length and head circumference by gestational age for girls
Gestational age	Weight	Length	Head circumference
40 weeks	7 lbs., 7.9 oz. (3.4 kg)	20 in. (51 cm)	13.8 in. (35 cm)
35 weeks	5 lbs., 4.7 oz. (2.4 kg)	17.7 in. (45 cm)	12.4 in. (31.5 cm)
32 weeks	3 lbs., 12 oz. (1.7 kg)	16.5 in. (42 cm)	11.4 in. (29 cm)
28 weeks	2 lbs., 3.3 oz. (1.0 kg)	14.1 in. (36 cm)	9.8 in. (25 cm)
24 weeks	1 lb., 5.2 oz. (0.60 kg)	12.6 in. (32 cm)	8.3 in. (21 cm)

Special care

If you deliver a preterm baby, your baby will likely need a longer hospital stay in a special nursery unit at the hospital. Depending on how much care your baby requires, he or she may be admitted to an intermediate care nursery or the neonatal intensive care unit (NICU). Doctors and a specialized team with training in taking care of preterm babies will be available to help care for your baby. Don’t hesitate to ask questions.

Your baby may need extra help feeding, and adapting immediately after delivery. Your health care team can help you understand what is needed and what your baby’s care plan will be.

Jaundice in premature babies

The most common type of jaundice among premature babies is exaggerated, physiologic jaundice. In this condition, the liver can’t rid the body of bilirubin. This substance is produced during the normal breakdown of red blood cells. As a result, bilirubin accumulates in the baby’s blood and spreads into the tissues. Because bilirubin is a yellowish color, the baby’s skin takes on a yellowish tint.

Jaundice is usually not a serious problem. However, if the bilirubin level gets too high, it can cause bilirubin toxicity. The substance can then build up in the brain and cause brain damage.

Ask your doctor or nurse for your baby’s bilirubin level. Normal levels of bilirubin in a newborn should be under 5 mg/dL. Many preterm babies, however, have bilirubin levels above that number. Bilirubin levels are not dangerous until they reach levels above 15-20 mg/dL, but phototherapy is generally started before levels get that high.

Treatment: The standard treatment for jaundice is phototherapy. This involves placing a baby under bright lights. The lights help break down the bilirubin into a substance that the body can get rid of more easily. Usually phototherapy is needed for less than a week. After that, the liver is mature enough to get rid of bilirubin on its own.

Kidney problems

A baby’s kidneys usually mature quickly after birth, but problems balancing the body’s fluids, salts, and wastes can occur during the first four to five days of life. This is especially true in babies less than 28 weeks into development. During this time, a baby’s kidneys may have difficulty:

• filtering wastesfrom the blood
• getting rid of wastes without excreting excess fluids
• producing urine

Because of the potential for kidney problems, neonatal intensive care unit (NICU) staff carefully record the amount of urine a baby produces. They may also test the blood for levels of potassium, urea, and creatinine.

Staff must also be watchful when giving medications, especially antibiotics. They need to make sure that the medicines are excreted from the body. If problems arise with kidney function, staff may need to restrict the baby’s fluid intake or give more fluids so that substances in the blood are not overly concentrated.

Treatment: The most common basic treatments are fluid restriction and salt restriction. Immature kidneys usually improve and have normal function within a few days.

Infections

A premature baby can develop infections in almost any part of the body. A baby may acquire an infection at any stage, ranging from in utero (while in the uterus), birthing through the genital tract, to after birth including the days or weeks in the NICU.

Regardless of when an infection is acquired, infections in premature infants are more difficult to treat for two reasons:

• A premature baby has a less developed immune system and fewer antibodies from the mother than a full-term baby. The immune system and antibodies are the body’s main defenses against infection.
• A premature baby often requires a number of medical procedures, including insertion of intravenous (IV) lines, catheters, and endotracheal tubes and possibly assistance from a ventilator. Each time a procedure is performed, there’s a chance of introducing bacteria, viruses, or fungi into the baby’s system.

If your baby has an infection, you may notice some or all of the following signs:

• lack of alertness or activity
• difficulty tolerating feedings
• poor muscle tone
• inability to maintain body temperature
• pale or spotted skin color, or a yellowish tint to the skin (jaundice)
• slow heart rate
• apnea (periods when the baby stops breathing)

These signs may be mild or dramatic, depending on the severity of the infection. As soon as there’s any suspicion that your baby has an infection, the NICU staff obtains samples of blood and often urine and spinal fluid to send to the laboratory for analysis.

Treatment: If there is evidence of infection, your baby may be treated with antibiotics, IV fluids, oxygen, or mechanical ventilation (help from a breathing machine). Although some infections can be serious, most babies respond well to treatments, including antibiotics if the infection is bacterial. The earlier your baby is treated, the better the chances of successfully fighting the infection.

Breathing problems

Breathing problems in premature babies are caused by an immature respiratory system. Immature lungs in premature babies often lack surfactant. This substance is a liquid that coats the inside of the lungs and helps keep them open. Without surfactant, a premature baby’s lungs can’t expand and contract normally. This increases their risk for respiratory distress syndrome.

Some premature babies also develop apnea and experience pauses in their breathing lasting for at least 20 seconds.

Some premature babies who lack surfactant may need to be put on a ventilator (breathing machine). Babies who are on a ventilator for a long time are at risk of developing a chronic lung condition called bronchopulmonary dysplasia. This condition causes fluid to build up in the lungs and increases the likelihood of lung damage.

Treatment: While being on a ventilator for an extended period of time may injure a baby’s lungs, it still may be necessary for the baby to receive continued oxygen therapy and ventilator support. Doctors may also use diuretic and inhaled medications.

Heart problems

The most common heart condition affecting premature babies is called apatent ductus arteriosus (PDA). The ductus arteriosus is the opening between two major blood vessels of the heart. In premature babies, the ductus arteriosus may remain open (patent) instead of closing as it should soon after birth. If this occurs, it can cause extra blood to be pumped through the lungs in the first days of life. Fluid can build up in the lungs, and heart failure can develop.

Treatment: Babies can be treated with the medication indomethacin, which causes the ductus arteriosus to close. If the ductus arteriosus remains open and symptomatic, an operation to close the duct may be required.

Brain problems

Brain problems can also occur in premature babies. Some premature babies have intraventricular hemorrhage, which is bleeding in the brain. Mild bleeding doesn’t usually cause permanent brain injury. However, heavy bleeding may result in permanent brain injury and cause fluid to accumulate in the brain. Severe bleeding can affect a baby’s cognitive and motor function.

Treatment: Treatment for brain problems can range from medication and therapy to surgery, depending on the severity of the problem.

RISK FACTOR-

Often, the specific cause of premature birth isn’t clear. However, there are known risk factors of premature delivery, including:

• Having a previous premature birth
• Pregnancy with twins, triplets or other multiples
• An interval of less than six months between pregnancies
• Conceiving through in vitro fertilization
• Problems with the uterus, cervix or placenta
• Smoking cigarettes or using illicit drugs
• Some infections, particularly of the amniotic fluid and lower genital tract
• Some chronic conditions, such as high blood pressure and diabetes
• Being underweight or overweight before pregnancy
• Stressful life events, such as the death of a loved one or domestic violence
• Multiple miscarriages or abortions
• Physical injury or trauma

For unknown reasons, black women are more likely to experience premature birth than are women of other races. But premature birth can happen to anyone. In fact, many women who have a premature birth have no known risk factors.

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

COMPLICATION-

While not all premature babies experience complications, being born too early can cause short-term and long-term health problems. Generally, the earlier a baby is born, the higher the risk of complications. Birth weight plays an important role, too.

Some problems may be apparent at birth, while others may not develop until later.

Short-term complications

In the first weeks, the complications of premature birth may include:

• Breathing problems. A premature baby may have trouble breathing due to an immature respiratory system. If the baby’s lungs lack surfactant — a substance that allows the lungs to expand — he or she may develop respiratory distress syndrome because the lungs can’t expand and contract normally. Premature babies may also develop a lung disorder known as bronchopulmonary dysplasia. In addition, some preterm babies may experience prolonged pauses in their breathing, known as apnea.
• Heart problems. The most common heart problems premature babies experience are patent ductus arteriosus (PDA) and low blood pressure (hypotension). PDA is a persistent opening between the aorta and pulmonary artery. While this heart defect often closes on its own, left untreated it can lead to a heart murmur, heart failure as well as other complications. Low blood pressure may require adjustments in intravenous fluids, medicines and sometimes blood transfusions.
• Brain problems. The earlier a baby is born, the greater the risk of bleeding in the brain, known as an intraventricular hemorrhage. Most hemorrhages are mild and resolve with little short-term impact. But some babies may have larger brain bleeding that causes permanent brain injury.
• Temperature control problems. Premature babies can lose body heat rapidly. They don’t have the stored body fat of a full-term infant, and they can’t generate enough heat to counteract what’s lost through the surface of their bodies. If body temperature dips too low, an abnormally low core body temperature (hypothermia) can result. Hypothermia in a premature baby can lead to breathing problems and low blood sugar levels. In addition, a premature infant may use up all of the energy gained from feedings just to stay warm. That’s why smaller premature infants require additional heat from a warmer or an incubator until they’re larger and able to maintain body temperature without assistance.
• Gastrointestinal problems. Premature infants are more likely to have immature gastrointestinal systems, resulting in complications such as necrotizing enterocolitis (NEC). This potentially serious condition, in which the cells lining the bowel wall are injured, can occur in premature babies after they start feeding. Premature babies who receive only breast milk have a much lower risk of developing NEC.
• Blood problems. Premature babies are at risk of blood problems such as anemia and newborn jaundice. Anemia is a common condition in which the body doesn’t have enough red blood cells. While all newborns experience a slow drop in red blood cell count during the first months of life, the decrease may be greater in premature babies. Newborn jaundice is a yellow discoloration in a baby’s skin and eyes that occurs because the baby’s blood contains excess bilirubin, a yellow-colored substance, from the liver or red blood cells. While there are many causes of jaundice, it is more common in preterm babies.
• Metabolism problems. Premature babies often have problems with their metabolism. Some premature babies may develop an abnormally low level of blood sugar (hypoglycemia). This can happen because premature infants typically have smaller stores of stored glucose than do full-term babies. Premature babies also have more difficulty converting their stored glucose into more-usable, active forms of glucose.
• Immune system problems. An underdeveloped immune system, common in premature babies, can lead to a higher risk of infection. Infection in a premature baby can quickly spread to the bloodstream, causing sepsis, an infection that spreads to the bloodstream.

Long-term complications

In the long term, premature birth may lead to the following complications:

• Cerebral palsy. Cerebral palsy is a disorder of movement, muscle tone or posture that can be caused by infection, inadequate blood flow or injury to a newborn’s developing brain either early during pregnancy or while the baby is still young and immature.
• Impaired learning. Premature babies are more likely to lag behind their full-term counterparts on various developmental milestones. Upon school age, a child who was born prematurely might be more likely to have learning disabilities.
• Vision problems. Premature infants may develop retinopathy of prematurity, a disease that occurs when blood vessels swell and overgrow in the light-sensitive layer of nerves at the back of the eye (retina). Sometimes the abnormal retinal vessels gradually scar the retina, pulling it out of position. When the retina is pulled away from the back of the eye, it’s called retinal detachment, a condition that, if undetected, can impair vision and cause blindness.
• Hearing problems. Premature babies are at increased risk of some degree of hearing loss. All babies will have their hearing checked before going home.
• Dental problems. Premature infants who have been critically ill are at increased risk of developing dental problems, such as delayed tooth eruption, tooth discoloration and improperly aligned teeth.
• Behavioral and psychological problems. Children who experienced premature birth may be more likely than full-term infants to have certain behavioral or psychological problems, as well as developmental delays.
• Chronic health issues. Premature babies are more likely to have chronic health issues — some of which may require hospital care — than are full-term infants. Infections, asthma and feeding problems are more likely to develop or persist. Premature infants are also at increased risk of sudden infant death syndrome (SIDS).

Long-term complications

Some premature birth complications are short-term and resolve within time. Others are long-term or permanent. Long-term complications include the following:

Cerebral palsy

Cerebral palsy is a movement disorder that affects muscle tone, muscle coordination, movement, and balance. It’s caused by an infection, poor blood flow, or a brain injury during pregnancy or after birth. Often, a specific cause can’t be determined.

Treatment: There is no cure for cerebral palsy, but treatments can help improve any limitations. Treatments include:

• assistive aids like eyeglasses, hearing aids, and walking aids
• medications to help with prevent muscle spasms, like diazepam and dantrolene
• surgery to improve mobility

• Parenthood
• Pregnancy

Premature Birth Complications

• Jaundice
• Kidney problems
• Infections
• Breathing problems
• Heart problems
• Brain problems
• Long-term complications
• Global impact
• Survival rate

Overview

A typical pregnancy lasts about 40 weeks, yet some babies arrive sooner. A premature birth is a birth that takes place before the 37th week of pregnancy.

While some premature babies have serious medical complications or long-term health problems, many also go on to live normal healthy lives. With modern medicine and new technologies, babies are often able to survive when born earlier during the pregnancy. The dedicated staff in hospital neonatal intensive care units (NICU) and advancements in neonatal care have also improved outcomes. These advancements include:

• family integrated care programs
• nutrition management
• skin-to-skin contact with premature babies
• efforts to reduce the number of infections in premature babies

While outcomes have improved for premature babies, complications can still occur. The following complications can affect preterm babies in the first weeks after birth.

Jaundice in premature babies

The most common type of jaundice among premature babies is exaggerated, physiologic jaundice. In this condition, the liver can’t rid the body of bilirubin. This substance is produced during the normal breakdown of red blood cells. As a result, bilirubin accumulates in the baby’s blood and spreads into the tissues. Because bilirubin is a yellowish color, the baby’s skin takes on a yellowish tint.

Jaundice is usually not a serious problem. However, if the bilirubin level gets too high, it can cause bilirubin toxicity. The substance can then build up in the brain and cause brain damage.

Ask your doctor or nurse for your baby’s bilirubin level. Normal levels of bilirubin in a newborn should be under 5 mg/dL. Many preterm babies, however, have bilirubin levels above that number. Bilirubin levels are not dangerous until they reach levels above 15-20 mg/dL, but phototherapy is generally started before levels get that high.

Treatment: The standard treatment for jaundice is phototherapy. This involves placing a baby under bright lights. The lights help break down the bilirubin into a substance that the body can get rid of more easily. Usually phototherapy is needed for less than a week. After that, the liver is mature enough to get rid of bilirubin on its own.

Kidney problems

A baby’s kidneys usually mature quickly after birth, but problems balancing the body’s fluids, salts, and wastes can occur during the first four to five days of life. This is especially true in babies less than 28 weeks into development. During this time, a baby’s kidneys may have difficulty:

• filtering wastesfrom the blood
• getting rid of wastes without excreting excess fluids
• producing urine

Because of the potential for kidney problems, neonatal intensive care unit (NICU) staff carefully record the amount of urine a baby produces. They may also test the blood for levels of potassium, urea, and creatinine.

Staff must also be watchful when giving medications, especially antibiotics. They need to make sure that the medicines are excreted from the body. If problems arise with kidney function, staff may need to restrict the baby’s fluid intake or give more fluids so that substances in the blood are not overly concentrated.

Treatment: The most common basic treatments are fluid restriction and salt restriction. Immature kidneys usually improve and have normal function within a few days.

Infections

A premature baby can develop infections in almost any part of the body. A baby may acquire an infection at any stage, ranging from in utero (while in the uterus), birthing through the genital tract, to after birth including the days or weeks in the NICU.

Regardless of when an infection is acquired, infections in premature infants are more difficult to treat for two reasons:

• A premature baby has a less developed immune system and fewer antibodies from the mother than a full-term baby. The immune system and antibodies are the body’s main defenses against infection.
• A premature baby often requires a number of medical procedures, including insertion of intravenous (IV) lines, catheters, and endotracheal tubes and possibly assistance from a ventilator. Each time a procedure is performed, there’s a chance of introducing bacteria, viruses, or fungi into the baby’s system.

If your baby has an infection, you may notice some or all of the following signs:

• lack of alertness or activity
• difficulty tolerating feedings
• poor muscle tone
• inability to maintain body temperature
• pale or spotted skin color, or a yellowish tint to the skin (jaundice)
• slow heart rate
• apnea (periods when the baby stops breathing)

These signs may be mild or dramatic, depending on the severity of the infection. As soon as there’s any suspicion that your baby has an infection, the NICU staff obtains samples of blood and often urine and spinal fluid to send to the laboratory for analysis.

Treatment: If there is evidence of infection, your baby may be treated with antibiotics, IV fluids, oxygen, or mechanical ventilation (help from a breathing machine). Although some infections can be serious, most babies respond well to treatments, including antibiotics if the infection is bacterial. The earlier your baby is treated, the better the chances of successfully fighting the infection.

Breathing problems

Breathing problems in premature babies are caused by an immature respiratory system. Immature lungs in premature babies often lack surfactant. This substance is a liquid that coats the inside of the lungs and helps keep them open. Without surfactant, a premature baby’s lungs can’t expand and contract normally. This increases their risk for respiratory distress syndrome.

Some premature babies also develop apnea and experience pauses in their breathing lasting for at least 20 seconds.

Some premature babies who lack surfactant may need to be put on a ventilator (breathing machine). Babies who are on a ventilator for a long time are at risk of developing a chronic lung condition called bronchopulmonary dysplasia. This condition causes fluid to build up in the lungs and increases the likelihood of lung damage.

Treatment: While being on a ventilator for an extended period of time may injure a baby’s lungs, it still may be necessary for the baby to receive continued oxygen therapy and ventilator support. Doctors may also use diuretic and inhaled medications.

Heart problems

The most common heart condition affecting premature babies is called apatent ductus arteriosus (PDA). The ductus arteriosus is the opening between two major blood vessels of the heart. In premature babies, the ductus arteriosus may remain open (patent) instead of closing as it should soon after birth. If this occurs, it can cause extra blood to be pumped through the lungs in the first days of life. Fluid can build up in the lungs, and heart failure can develop.

Treatment: Babies can be treated with the medication indomethacin, which causes the ductus arteriosus to close. If the ductus arteriosus remains open and symptomatic, an operation to close the duct may be required.

Brain problems

Brain problems can also occur in premature babies. Some premature babies have intraventricular hemorrhage, which is bleeding in the brain. Mild bleeding doesn’t usually cause permanent brain injury. However, heavy bleeding may result in permanent brain injury and cause fluid to accumulate in the brain. Severe bleeding can affect a baby’s cognitive and motor function.

Treatment: Treatment for brain problems can range from medication and therapy to surgery, depending on the severity of the problem.ADVERTISEMENTGet answers from an OB-GYN in minutes, anytime

Have medical questions? Connect with an experienced, board-certified gynecologist online or by phone. Pediatricians and other specialists also available 24/7.

Long-term complications

Some premature birth complications are short-term and resolve within time. Others are long-term or permanent. Long-term complications include the following:

Cerebral palsy

Cerebral palsy is a movement disorder that affects muscle tone, muscle coordination, movement, and balance. It’s caused by an infection, poor blood flow, or a brain injury during pregnancy or after birth. Often, a specific cause can’t be determined.

Treatment: There is no cure for cerebral palsy, but treatments can help improve any limitations. Treatments include:

• assistive aids like eyeglasses, hearing aids, and walking aids
• medications to help with prevent muscle spasms, like diazepam and dantrolene
• surgery to improve mobility

Vision problems

Premature babies are at risk for retinopathy of prematurity. In this condition, blood vessels in the back of the eye become swollen. This can cause gradual retina scarring and retinal detachment, increasing the risks of vision loss or blindness.

Treatment: If retinopathy is severe, some of the following treatments may be used:

• cryosurgery, which involves freezing and destroying abnormal blood vessels in the retina
• laser therapy, which uses powerful light beams to burn and eliminate abnormal vessels
• vitrectomy, which is a surgery to remove scar tissue from the eye
• scleral buckling surgery, which consists of placing a flexible band around the eye to prevent retinal detachment

Hearing problems

Some premature babies experience some hearing loss. Hearing loss can sometimes be total, causing deafness. Many times, the exact cause hearing loss in premature babies is unknown.

Your baby will have their hearing tested in the hospital or shortly after discharge. Some of the later signs that your baby may have hearing loss are:

• not being startled by loud sounds
• not imitating sounds by six months of age
• not babbling by one year of age
• not turning at the sound of your voice

Treatment: Depending on the cause of hearing loss in your baby, treatments will vary. Treatments can include:

• surgery
• ear tubes
• hearing aid
• cochlear implant

Dental problems

Dental issues can affect a premature baby later in life. These include tooth discoloration, delayed tooth growth, or improper alignment.

Treatment: A pediatric dentist can help correct these problems.

Behavioral problems

Children born prematurely are more likely to have behavioral or psychological problems. These include attention-deficit disorder (ADD) and attention-deficit/hyperactivity disorder (ADHD).

Treatment: Creating a structured and consistent schedule plus medication, like Ritalin or Adderall, can help kids with ADHD.

Impaired cognitive function

Premature babies are also at greater risk for long-term disabilities, which can be intellectual, developmental, or both. These children may develop at a slower rate than babies born full-term.

Chronic health problems

In addition, premature babies have a greater risk for chronic health problems. They are more susceptible to infections, and may suffer from other problems such as asthma or difficulty feeding. There’s also an increased risk of sudden infant death syndrome (SIDS) among premature infants.

PREVENTION-

Although the exact cause of preterm birth is often unknown, there are some things that can be done to help women — especially those who have an increased risk — to reduce their risk of preterm birth, including:

• Progesterone supplements. Women who have a history of preterm birth, a short cervix or both factors may be able to reduce the risk of preterm birth with progesterone supplementation.
• Cervical cerclage. This is a surgical procedure performed during pregnancy in women with a short cervix, or a history of cervical shortening that resulted in a preterm birth.

MANAGEMENT-

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

Premature babies often need time to catch up in both development and growth. In the hospital, this catch-up time may mean learning to eat and sleep, as well as steadily gaining weight. Babies may stay in the hospital until they reach the pregnancy due date. They may be cared for in a neonatal intensive care unit (NICU).

Talk with your baby’s healthcare provider about when your baby will be able to go home. In general, babies can go home when they:

• Have no serious health conditions
• Can stay warm in an open crib
• Take all feedings by breast or bottle, maintaining their expected growth rate
• Have no recent periods of not breathing (apnea) or low heart rate

Before discharge, premature babies need an eye exam and hearing test to check for problems related to prematurity. You must be able to give care, including medicines and feedings, before your baby can go home. You will also need information about follow-up visits with the baby’s healthcare provider and vaccines. Many hospitals have special follow-up healthcare programs for premature and low-birth-weight babies.

Even though they are otherwise ready to go home, some babies still have special needs. This includes things such as extra oxygen or tube feedings. You will learn how to take care of your baby if he or she needs these things. Hospital staff can help set up special home care.

Ask your baby’s healthcare provider about staying overnight in a parenting room at the hospital before your baby goes home. This can help you adjust to caring for your baby while healthcare providers are nearby for help and reassurance. You may also feel more confident taking your baby home when you know infant CPR and safety.

Premature babies are at increased risk for sudden infant death syndrome (SIDS). You should always put your baby down to sleep on his or her back.

WHO response

In 2012, WHO and partners published a report Born too soon: the global action report on preterm birth that included the first-ever estimates of preterm birth by country.

WHO is committed to reducing the health problems and lives lost as a result of preterm birth:

• Working with Member States and partners to implement Every newborn: An action plan to end preventable deaths adopted in May 2014 in the framework of the UN Secretary-General’s Global strategy for women’s and children’s health;
• Working with Member States to strengthen the availability and quality of data on preterm births;
• Providing updated analyses of global preterm birth levels and trends every 3 to 5 years;
• Working with partners around the world to conduct research into the causes of preterm birth, and test effectiveness and delivery approaches for interventions to prevent preterm birth and treat babies that are born preterm;
• Regularly updating clinical guidelines for the management of pregnancy and mothers with preterm labour or at risk of preterm birth, and guidelines on the care of preterm babies, including kangaroo mother care, feeding babies with low birth weight, treating infections and respiratory problems, and home-based follow-up care (see WHO 2015 recommendations on interventions to improve preterm outcomes);
• Developing tools to improve health workers’ skills and assess the quality of care provided to mothers at risk of preterm delivery and preterm babies; and
• Supporting countries to implement WHO’s antenatal care guidelines, aimed at reducing the risk of negative pregnancy outcomes, including preterm births, and ensuring a positive pregnancy experience for all women.

In 2019, WHO and UNICEF published Survive and thrive: transforming care for every small and sick newborn. This report highlights how countries can strengthen care to support babies born too small or too soon, including through increased investment, round the clock care for newborns and better partnership with families.

Guidelines to improve preterm birth outcomes

WHO has developed new guidelines with recommendations for improving outcomes of preterm births. This set of key interventions can improve the chances of survival and health outcomes for preterm infants. The guidelines include interventions provided to the mother – for example steroid injections before birth, antibiotics when her water breaks before the onset of labour, and magnesium sulfate to prevent future neurological impairment of the child – as well as interventions for the newborn baby – for example thermal care, feeding support, kangaroo mother care, safe oxygen use, and other treatments to help babies breathe more easily.

• WHO recommendations on interventions to improve preterm birth outcomes

---

WHO is currently coordinating two clinical trials, called the WHO ACTION Trials (Antenatal Corticosteroids for Improving Outcomes in preterm Newborns) for women at risk of preterm birth by:

• Immediate kangaroo mother care (KMC) multi-country trial (compared with the current recommendations of initiating KMC when baby is stable) in Ghana, India, Malawi, Nigeria and the United Republic of Tanzania.
• Implementation research to scale-up KMC in India and Ethiopia.

The trials will assess how steroid injections can be used safely and effectively for women and preterm newborns in low- and middle-income countries.

FOR MORE INFO- CLICK – https://www.who.int/news-room/fact-sheets/detail/preterm-birth

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

---

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

INTRODUCTION-

Urinary incontinence happens when you lose control of your bladder. In some cases, you may empty your bladder’s contents completely. In other cases, you may experience only minor leakage. The condition may be temporary or chronic, depending on its cause.

According to the Urology Care Foundation, millions of adults in the United States experience urinary incontinence. According to Johns Hopkins Medicine, it’s more common among women age 50 and over. However, this condition can affect anyone.

As you age, the muscles supporting your bladder tend to weaken, which can lead to urinary incontinence.

Many different health problems can also cause the condition. Symptoms can range from mild to severe and can be a sign of cancer, kidney stones, infection, or an enlarged prostate.

If you experience urinary incontinence, make an appointment with your healthcare provider. Urinary incontinence can interfere with your daily life and lead to potential accidents. Your healthcare provider can also determine if a more serious medical condition is the cause.

Urinary incontinence — the loss of bladder control — is a common and often embarrassing problem. The severity ranges from occasionally leaking urine when you cough or sneeze to having an urge to urinate that’s so sudden and strong you don’t get to a toilet in time.

Though it occurs more often as people get older, urinary incontinence isn’t an inevitable consequence of aging. If urinary incontinence affects your daily activities, don’t hesitate to see your doctor. For most people, simple lifestyle changes or medical treatment can ease discomfort or stop urinary incontinence.

TYPES-

Urinary incontinence is divided into three general types. You can potentially experience more than one type at the same time.

Stress incontinence

Stress incontinence is triggered by certain types of physical activity.

For example, you might lose control of your bladder when you’re:

• exercising
• coughing
• sneezing
• laughing

Such activities put stress on the sphincter muscle that holds urine in your bladder. The added stress can cause the muscle to release urine.

Urge incontinence

Urge incontinence occurs when you lose control of your bladder after experiencing a sudden and strong urge to urinate. Once that urge hits, you may not be able to make it to the bathroom in.

Overflow incontinence

Overflow incontinence can occur if you don’t completely empty your bladder when you urinate. Later, some of the remaining urine may leak from your bladder. This type of incontinence is sometimes called “dribbling.”

Mixed Incontinence

Some people have more than one type of urinary incontinence. Some people leak urine both with strong physical activity (SUI) AND have a strong uncontrollable sense of urgency (OAB.) This is mixed urinary incontinence. This person has both SUI and OAB. In this case, it helps to know what is occurring and what is causing leaks to learn how to manage problems.

CAUSES-

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

Urinary incontinence isn’t a disease, it’s a symptom. It can be caused by everyday habits, underlying medical conditions or physical problems. A thorough evaluation by your doctor can help determine what’s behind your incontinence.

Temporary urinary incontinence

Certain drinks, foods and medications may act as diuretics — stimulating your bladder and increasing your volume of urine. They include:

• Alcohol
• Caffeine
• Carbonated drinks and sparkling water
• Artificial sweeteners
• Chocolate
• Chili peppers
• Foods that are high in spice, sugar or acid, especially citrus fruits
• Heart and blood pressure medications, sedatives, and muscle relaxants
• Large doses of vitamin C

Urinary incontinence may also be caused by an easily treatable medical condition, such as:

• Urinary tract infection. Infections can irritate your bladder, causing you to have strong urges to urinate, and sometimes incontinence.
• Constipation. The rectum is located near the bladder and shares many of the same nerves. Hard, compacted stool in your rectum causes these nerves to be overactive and increase urinary frequency.

Persistent urinary incontinence

Urinary incontinence can also be a persistent condition caused by underlying physical problems or changes, including:

• Pregnancy. Hormonal changes and the increased weight of the fetus can lead to stress incontinence.
• Childbirth. Vaginal delivery can weaken muscles needed for bladder control and also damage bladder nerves and supportive tissue, leading to a dropped (prolapsed) pelvic floor. With prolapse, the bladder, uterus, rectum or small intestine can get pushed down from the usual position and protrude into the vagina. Such protrusions can be associated with incontinence.
• Changes with age. Aging of the bladder muscle can decrease the bladder’s capacity to store urine. Also, involuntary bladder contractions become more frequent as you get older.
• Menopause. After menopause women produce less estrogen, a hormone that helps keep the lining of the bladder and urethra healthy. Deterioration of these tissues can aggravate incontinence.
• Hysterectomy. In women, the bladder and uterus are supported by many of the same muscles and ligaments. Any surgery that involves a woman’s reproductive system, including removal of the uterus, may damage the supporting pelvic floor muscles, which can lead to incontinence.
• Enlarged prostate. Especially in older men, incontinence often stems from enlargement of the prostate gland, a condition known as benign prostatic hyperplasia.
• Prostate cancer. In men, stress incontinence or urge incontinence can be associated with untreated prostate cancer. But more often, incontinence is a side effect of treatments for prostate cancer.
• Obstruction. A tumor anywhere along your urinary tract can block the normal flow of urine, leading to overflow incontinence. Urinary stones — hard, stone-like masses that form in the bladder — sometimes cause urine leakage.
• Neurological disorders. Multiple sclerosis, Parkinson’s disease, a stroke, a brain tumor or a spinal injury can interfere with nerve signals involved in bladder control, causing urinary incontinence.

There are many potential causes of urinary incontinence.

Examples include:

• weakened bladder muscles, resulting from aging
• physical damage to your pelvic floor muscles
• enlarged prostate
• cancer

Some of these conditions are easily treatable and only cause temporary urinary problems. Others are more serious and persistent.

Aging

As you get older, the muscles supporting your bladder typically become weaker, which raises your risk for incontinence.

To maintain strong muscles and a healthy bladder, it’s important to practice healthy lifestyle habits. The healthier you are, the better your chances of avoiding incontinence as you age.

Damage

Your pelvic floor muscles support your bladder. Damage to these muscles can cause incontinence. It can be caused by certain types of surgery, such as a hysterectomy. It’s also a common result of pregnancy and childbirth.

Enlarged prostate

If you’re male, your prostate gland surrounds the neck of your bladder. This gland releases fluid that protects and nourishes your sperm. It tends to enlarge with age. It’s common for males to experience some incontinence as a result.

Cancer

Prostate or bladder cancer can cause incontinence. In some cases, treatments for cancer can also make it harder for you to control your bladder. Even benign tumors can cause incontinence by blocking your flow of urine.

Other potential causes

Other potential causes of incontinence include:

• constipation
• urinary tract infections (UTIs)
• kidney or bladder stones
• prostatitis, or inflammation of your prostate
• interstitial cystitis, or a chronic condition that causes inflammation within your bladder
• side effects from certain medications, such as blood pressure drugs, muscle relaxants, sedatives, and some heart medications

Some lifestyle factors can also cause temporary bouts of incontinence. For example, drinking too much alcohol, caffeinated beverages, or other fluids can cause you to temporarily lose control of your bladder.

DIAGNOSIS-

A urologist or primary care doctor will start by asking questions. They will want to know about your symptoms and your medical history. They will ask about your health habits and fluid intake. They will also want to know how much your incontinence has changed your quality of life.

A good medical history, physical exam and a few simple tests are most often all that is needed to diagnose the cause of incontinence. A complete review of the medications you are taking may reveal one that alters normal bladder or urethral function. Your doctor may test your urine for bacteria or blood (urinalysis) to look for a urinary tract infection or other source of irritation to the bladder.

A cough stress test may be performed to check for SUI. A simple bladder ultrasound test to see how well you empty your bladder is often performed. Or a more involved “stress test” for the bladder can be done in more complicated cases (urodynamic test) to better see just how your bladder and urethra work. Other conditions to look for include vaginal hernias or pelvic organ prolapse (POP), and major bowel problems, such as constipation or fecal incontinence.

A urologist or primary care doctor will start by asking questions. They will want to know about your symptoms and your medical history. They will ask about your health habits and fluid intake. They will also want to know how much your incontinence has changed your quality of life.

A good medical history, physical exam and a few simple tests are most often all that is needed to diagnose the cause of incontinence. A complete review of the medications you are taking may reveal one that alters normal bladder or urethral function. Your doctor may test your urine for bacteria or blood (urinalysis) to look for a urinary tract infection or other source of irritation to the bladder.

A cough stress test may be performed to check for SUI. A simple bladder ultrasound test to see how well you empty your bladder is often performed. Or a more involved “stress test” for the bladder can be done in more complicated cases (urodynamic test) to better see just how your bladder and urethra work. Other conditions to look for include vaginal hernias or pelvic organ prolapse (POP), and major bowel problems, such as constipation or fecal incontinence.

A cough stress test may be performed to check for SUI. A simple bladder ultrasound test to see how well you empty your bladder is often performed. Or a more involved “stress test” for the bladder can be done in more complicated cases (urodynamic test) to better see just how your bladder and urethra work. Other conditions to look for include vaginal hernias or pelvic organ prolapse (POP), and major bowel problems, such as constipation or fecal incontinence.

Risk factors

Factors that increase your risk of developing urinary incontinence include:

• Gender. Women are more likely to have stress incontinence. Pregnancy, childbirth, menopause and normal female anatomy account for this difference. However, men with prostate gland problems are at increased risk of urge and overflow incontinence.
• Age. As you get older, the muscles in your bladder and urethra lose some of their strength. Changes with age reduce how much your bladder can hold and increase the chances of involuntary urine release.
• Being overweight. Extra weight increases pressure on your bladder and surrounding muscles, which weakens them and allows urine to leak out when you cough or sneeze.
• Smoking. Tobacco use may increase your risk of urinary incontinence.
• Family history. If a close family member has urinary incontinence, especially urge incontinence, your risk of developing the condition is higher.
• Other diseases. Neurological disease or diabetes may increase your risk of incontinence.

Complications

Complications of chronic urinary incontinence include:

• Skin problems. Rashes, skin infections and sores can develop from constantly wet skin.
• Urinary tract infections. Incontinence increases your risk of repeated urinary tract infections.
• Impacts on your personal life. Urinary incontinence can affect your social, work and personal relationships.

Prevention

Urinary incontinence isn’t always preventable. However, to help decrease your risk:

• Maintain a healthy weight
• Practice pelvic floor exercises
• Avoid bladder irritants, such as caffeine, alcohol and acidic foods
• Eat more fiber, which can prevent constipation, a cause of urinary incontinence
• Don’t smoke, or seek help to quit smoking

TREATMENT-

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

There are many ways to help you take control over your bladder. You may not need to wear pads or diapers. Some problems are short-term and can be easily relieved. Others take more time to treat. Treatments range from lifestyle changes to bladder training to medications to simple procedural therapies to surgery.

Lifestyle Changes

Lifestyle changes, such as changing your diet, should be tried first. With lifestyle changes, you change the way you live day-to-day. This may include what you eat or drink, or practicing other methods that may control symptoms. You may not get rid of all symptoms with lifestyle changes, but your symptoms may feel better after changing a few habits. For some, weight loss has been linked to helping urinary symptoms.

Fluid Control

You will likely be asked to track what you drink, when and how much. You may learn that you should limit certain things such as caffeine and alcohol. These drinks may bother the bladder. You may also be asked to drink more water. Six to eight glasses of water per day is ideal. Also, you may be asked not to drink for a few hours before bed. This will help reduce your need to get up and go to the bathroom at night.

Limit Certain Foods and Drinks

Some foods and drinks have been found, anecdotally, as irritants to the bladder. Some people have found spicy foods, coffee, tea and colas to be bothersome. However, studies have not proven that these are really “bladder irritants” in all patients. A good plan is for you to try to notice on your own how different food and drinks effect you and your symptoms.

Bladder Training

A bladder diary is the starting point for bladder training. For 3 days, you write down what and how much you drink, and how often you go to the bathroom. Noting when you leak urine can also be helpful. This diary can help you and your provider find things that may make your symptoms worse. It can also help your provider build a bladder training plan for you. This is when you empty your bladder in a controlled way at set times. When you empty your bladder as a routine, you should have less leaks. Timed urination, scheduled voiding or double voiding are methods that can help with both OAB and SUI.

If you go to the bathroom too often, retraining your bladder can help. The goal is to hold your urine in the bladder for longer and longer amounts of time. This takes small steps. Start with adding 5 to 10 minutes. The goal is to retrain your bladder to hold urine for 3 to 4 hours, with less urgency and leaking.

Pelvic Floor Exercises

Kegel exercises can strengthen the urethral sphincter and pelvic floor muscles. This works for both men and women. If you can learn to tighten and relax these muscles, this can often help your bladder control.

Kegels can also help control the bladder spasms that trigger the urge to go. Squeezing the pelvic floor muscles inspires a reflex to the bladder to get the bladder to quiet down, to help suppress the urge feeling. This can pause or even stop the uncontrollable UUI leaks. A health care provider can teach you how to do these exercises with success.

Kegels can help with both SUI (by making the muscles strong) and OAB/UUI (by suppressing the urge feeling). Like any fitness program, you must practice the exercises often to keep helping your body.

Medical Treatments

When lifestyle changes do not help enough, your health care provider may ask you to try prescription medications. A frank talk with your provider about the risks, side effects and benefits of each medication will help you decide which might be the right one for you.

Anticholinergic Drugs

Anticholinergic drugs treat OAB/UUI by helping the bladder muscle to relax. Common medications include oxybutynin, tolterodine and solifenacin. They work well for the bladder, but are also linked to many bothersome side effects such as dry mouth, constipation, blurred vision, and lately, some concern for causing confusion or dementia with longer-term use. Trospium chloride does not diffuse into the brain so is not thought to have a risk of confusion or dementia.

A newer medication for OAB is merbegron. It is not an anticholinergic medication, so it is not linked to any of the side effects described above. It is an alpha-agonist, so works a little differently on the bladder, but in the end has the same effect of getting the bladder to relax. It can cause increases in blood pressure so needs to be used with caution in patients with hypertension.

Be sure to talk about any bladder relaxing drugs you have tried when you talk with your urologist.

Hormone Treatment

For women, local vaginal/urethral estrogen therapy can help if you are having urinary incontinence after menopause. Estrogen replacement helps the health of the walls of the vagina, the bladder neck and the urethra. This may ease irritative bladder symptoms and incontinence. There are some special medical reasons not to use local hormones, so be sure to speak to your provider about what is best for you.

Surgical Treatments for SUI

Choosing to have surgery is very personal. If surgery is suggested, there are many choices. It helps to learn as much as you can before you decide. You should work with a doctor who has experience in SUI surgery. Learn the risks and benefits of all your surgical choices, as well as what to expect during and after surgery, to make the most informed choice that will be best for you.

Slings

• Female Sling

The most common surgical treatment and the current standard of care for the surgical treatment of female SUI is the midurethral sling surgery. For this, a strip of soft permanent mesh is placed under the urethra to support urethral closure during actions that involve “physical pelvic stress” (coughing, sneezing, bending, lifting, jumping and running). It is a simple 10-20 minute, outpatient procedure with a small single-cut in the vagina. This is easily done under limited anesthesia and linked to a very quick return to normal day-to-day activities. Long-term success rates are in the 90%.

Another type of female sling surgery, the pubovaginal sling, is a bladder neck sling. Here the tissue used to make the sling comes from the patient’s abdominal wall (fascia), or donated tissue (bovine or cadaver).

• Male Sling

A sling procedure may be offered to treat SUI in some men. The male sling is for urethral sphincter muscle support. For this, a soft mesh tape is placed under the urethra through a cut between the scrotum and rectum. It supports the urethra and sphincter muscle by pushing up on the urethra and causing some coaptation (closure) of the urethra to prevent leaks. Ask your healthcare provider if this is an option for you.

Bladder Neck Suspension / Colposuspension

The Burch Colposuspension, or bladder neck suspension, is surgery for female SUI that lifts the bladder neck up towards the pubic bone with permanent stitches. This is a bigger surgery with a cut through the abdominal wall (muscles and skin), to reach the deeper pelvic areas. Because of the cut into the belly, it takes a longer time to heal from this surgery compared to the more minimally invasive midurethral sling, but it can be the right choice for some patients. In some cases it can be performed laparoscopically, which lessens the recovery time after surgery.

Bulking Agents (Injections)

This option is used to treat female SUI by “bulking up” the inner urethral lining and making the opening of the urethra smaller. Modern bulking agents are permanent materials that are placed into the tissues around the urethra and sphincter muscle up towards the bladder neck. This helps how well the natural urethral closure function can work to stop leaks.

Note that bulking agents are not FDA-approved for male SUI.

Artificial Urinary Sphincter

The most common treatment for male SUI is to implant a device around the urethra called an artificial urinary sphincter (AUS). In some cases, women may also be helped from this surgery, but due to other surgical options mentioned earlier, this is rarely needed in women. The AUS is a device with three parts:

1. An artificial urinary sphincter, which is a fluid filled cuff placed around the urethra.
2. A fluid-filled, pressure-sensing balloon that joins to the cuff and regulates the pressure within the cuff. This balloon is placed in the lower abdomen.
3. A pump placed in the scrotum for men (and labia for women), that transfers the fluid between the cuff and the balloon to open and close the cuff (artificial urinary sphincter). The pump is easily controlled by the patient.

At rest, the AUS cuff is closed (full of fluid) to prevent leaks. When you decide to empty your bladder, you activate the pump to push fluid from the cuff to the balloon that holds your urine. This allows the urethra to open so that the urine can flow through and empty the bladder. This surgery can cure or greatly help urinary control in about 70-80% of men. If you have had radiation, scar tissue in the urethra, or other bladder problems then this option may not be the best option for you.

Surgical Treatments for OAB

If lifestyle changes and medicine are not working for your OAB, there are other options. A trained urologist or female pelvic medicine & reconstructive surgery (FPMRS) specialist can help.

Bladder Botox® Treatment

Your doctor may offer bladder Botox® (onabotulinumtoxin). Botox works for the bladder to relax the muscle of the bladder wall to reduce urinary urgency and urge incontinence. To put Botox into the bladder your doctor will use a small camera, a cystoscope, through the urethra and into the bladder. With a tiny needle attached to the cystoscope, the Botox is injected in small amounts straight into the wall of the bladder, spreading it out evenly throughout the bladder. This procedure is most often performed in the office with local anesthesia (numbing mixture in the bladder). The effects of Botox last about 6-9 months, so repeat treatments will be needed when OAB symptoms return.

Within a few weeks of the treatment, your health care provider will want to check to see how well it is working for you, and to make sure you are still able to empty your bladder well. A small amount (<10%) of patients have trouble emptying their bladder for a short time after the treatment and may need to use a catheter (small tube) until their voiding improves.

Nerve Stimulation

Another treatment for people who need extra help for their OAB is nerve stimulation, also called neuromodulation therapy. This type of treatment sends electrical pulses to nerves that share the same path for the bladder (pelvic nerves). In OAB, the nerve signals between your bladder and brain do not always communicate the right way. Treatment with electrical pulses help to modulate the neurological signaling so the brain and the pelvic nerves can communicate better to help the bladder function – to “calm down” — and help OAB symptoms.

There are two main types available today:

• Percutaneous Tibial Nerve Stimulation (PTNS)

Percutaneous Tibial Nerve Stimulation, or PTNS, (peripheral) is an easy way to modulate the nerves to your bladder. PTNS is performed in the office, with each session taking about 30 minutes. PTNS is done by placing a small needle electrode in your lower leg near your ankle. It sends stimulation pulses up the leg, by way of the tibial nerve, to the pelvic nerves that modulate the bladder function to “calm the bladder down.” The therapy is approved as a program of weekly 30 minute sessions for 12 treatments, followed by on-going monthly care treatment sessions to keep the benefits.

• Sacral Nerve Stimulation (SNS)

SNS (central) stimulates the pelvic nerves by way of direct sacral nerve stimulation – the nerve root coming right off the spinal cord. Stimulation here again serves to modulate the neurological signaling between the bladder and the brain to help bladder function. SNS involves an implantable bladder pacemaker to control these signals to stop OAB symptoms. SNS is a two-step surgical process, which gives patients the chance to try the therapy first before making choices about final surgical implantation of the pacemaker. The first step is to implant an electrical wire through the skin in your lower back that goes deep towards the sacral nerves. This wire is linked to an external, handheld pacemaker for the test. If it helps sufficiently for your OAB symptoms, the second step is to join the wire to an implantable permanent pacemaker. The stimulation is then continuous as it regulates the pelvic nerve activity to control the OAB symptoms.

Bladder Reconstruction / Urinary Diversion Surgery

These type of major abdominal surgeries are only used in very rare and complicated cases. There are two main categories of major abdominal surgery. The goal of augmentation cystoplasty is to make the bladder bigger to increase how much urine it can hold at any one time. The goal of urinary diversion is to re-route the flow of urine away from the bladder and often results in a stoma and external appliance to catch the urine. There are many risks to these surgeries, so it is offered only when no other option can help.

Surgical Treatments for Overflow Incontinence

Overflow urinary incontinence happens when the bladder cannot empty well and dribbles as the bladder pressure grows. Most often, it is linked to some type of block of the bladder neck and/or urethra, and requires some type of procedural or surgical action to fix the block. Common problems in men that can lead to holding urine in and overflow incontinence include an enlarged prostate (benign prostatic hyperplasia, BPH) and urethral strictures. It is quite rare for urethral strictures to happen in women. Other medical problems can change how the bladder contracts to empty, which can also lead to overflow incontinence.

You should speak with your urologist to learn what therapy might be right for you.

Products and Devices

For some people, incontinence products and devices are the only way to manage bladder problems to give you more freedom to do the things you want to do.

Some include:

• Indwelling catheter (stays in your body day and night, joined to a drainage bag)
• Intermittent catheters that are used many times each day
• External collecting systems (condom style for men, funnel and pouch for women)
• Absorbent products (pads, adult diapers, tampons)
• Pessaries for women, mostly those designed for SUI
• Toilet substitutes (like portable commodes)

Whatever your urinary problem is, there are likely good choices for you. It is vital to find a provider that specializes in bladder and incontinence problems, such as a urologist.

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

Pelvic floor dysfunction is the inability to correctly relax and coordinate your pelvic floor muscles to have a bowel movement. Symptoms include constipation, straining to defecate, having urine or stool leakage and experiencing a frequent need to pee. Initial treatments include biofeedback, pelvic floor physical therapy and medications.

INTRODUCTION-

Pelvic floor dysfunction is a common condition where you’re unable to correctly relax and coordinate the muscles in your pelvic floor to urinate or to have a bowel movement. If you’re a woman, you may also feel pain during sex, and if you’re a man you may have problems having or keeping an erection (erectile dysfunction or ED). Your pelvic floor is a group of muscles found in the floor (the base) of your pelvis (the bottom of your torso).

If you think of the pelvis as being the home to organs like the bladder, uterus (or prostate in men) and rectum, the pelvic floor muscles are the home’s foundation. These muscles act as the support structure keeping everything in place within your body. Your pelvic floor muscles add support to several of your organs by wrapping around your pelvic bone. Some of these muscles add more stability by forming a sling around the rectum.

The pelvic organs include:

• The bladder (the pouch holding your urine).
• The uterus and vagina (in women).
• The prostate (in men).
• The rectum (the area at the end of the large intestine where your body stores solid waste).

Normally, you’re able to go to the bathroom with no problem because your body tightens and relaxes its pelvic floor muscles. This is just like any other muscular action, like tightening your biceps when you lift a heavy box or clenching your fist.

But if you have pelvic floor dysfunction, your body keeps tightening these muscles instead of relaxing them like it should. This tension means you may have:

• Trouble evacuating (releasing) a bowel movement.
• An incomplete bowel movement.
• Urine or stool that leaks.

As many as 50 percent of people with chronic constipation have pelvic floor dysfunction (PFD) — impaired relaxation and coordination of pelvic floor and abdominal muscles during evacuation. Straining, hard or thin stools, and a feeling of incomplete elimination are common signs and symptoms. But because slow transit constipation and functional constipation can overlap with PFD, some patients may also present with other signs and symptoms, such as a long time between bowel movements and abdominal pain.

When mechanical, anatomic, and disease- and diet-related causes of constipation have been ruled out, clinical suspicion should be raised to the possibility that PFD is causing or contributing to constipation. A focused history and digital examination are key components in diagnosing PFD. The diagnosis can be confirmed by anorectal manometry with balloon expulsion and, in some cases, traditional proctography or dynamic magnetic resonance imaging defecography to visualize pathologic pelvic floor motion, sphincter anatomy and greater detail of surrounding structures.

To help patients restore normal bowel function, Mayo Clinic staff use a multidisciplinary approach that can include:

• Constipation education classes led by a dietitian and a nurse educator
• Intensive pelvic floor retraining exercises
• Biofeedback training
• Behavior modification

Patients may meet individually with a dedicated nurse educator who provides a focused session on bowel management techniques. Central to the process is a daily regimen that combines an evening dose of fiber supplement with a morning routine of mild physical activity; a hot, preferably caffeinated beverage; and, possibly, a fiber cereal followed by another cup of a hot beverage — all within 45 minutes of waking. This routine augments early morning high-amplitude peristaltic contractions by incorporating multiple colon stimulators.

The regimen, useful for many types of constipation, is fine-tuned for PFD. Some patients do not need fiber; others may need to supplement with occasional laxatives. The program can change over time as patients make advancements.

Biofeedback to retrain pelvic floor muscles

Once patients with pelvic floor constipation have these basic tools, they can begin retraining the pelvic floor muscles with biofeedback. Based on the principle of operant conditioning, biofeedback provides auditory and visual feedback to help retrain the pelvic floor and relax the anal sphincter. Biofeedback training is the treatment of choice for medically refractory pelvic floor constipation, with some studies showing improvement in more than 70 percent of patients. Patients also learn to identify internal sensations associated with relaxation and long-term skills and exercises for use at home.

Although many centers are familiar with retraining techniques to improve pelvic floor dysfunction, few have the multidisciplinary expertise to teach patients with constipation how to appropriately coordinate abdominal and pelvic floor muscles during defecation, and how to use bowel management techniques, along with behavior modification, to relieve symptoms. Because pelvic floor dysfunction can be associated with psychological, sexual or physical abuse and other life stressors, psychological counseling is often included in the evaluation process.

CAUSES-

While exact causes are still being researched, doctors can link pelvic floor dysfunction to conditions or events that weaken the pelvic muscles or tear connective tissue:

• childbirth
• traumatic injury to the pelvic region
• obesity
• pelvic surgery
• nerve damage

The full causes of pelvic floor dysfunction are still unknown. But a few of the known factors include:

• Traumatic injuries to the pelvic area (like a car accident).
• Pregnancy.
• Overusing the pelvic muscles (like going to the bathroom too often or pushing too hard), eventually leading to poor muscle coordination.
• Pelvic surgery.
• Being overweight.
• Advancing age.

Does pregnancy cause pelvic floor dysfunction?

Pregnancy is a common cause of pelvic floor dysfunction. Often women get experience pelvic floor dysfunction after they give birth. Your pelvic floor muscles and tissues can become strained during pregnancy, especially if your labor was long or difficult.

Is pelvic floor dysfunction hereditary?

Pelvic floor dysfunction can run in your family. This is called a hereditary condition. Researchers are looking into a potential genetic cause of pelvic floor dysfunction.

SIGN AND SYMPTOM-

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

There are a few well-known signs and symptoms that people experience when they have a problem with their pelvic floor muscles. The following list of signs and symptoms are common for people with weak pelvic floor muscles. Urinary dysfunction, erectile dysfunction, premature ejaculation, painful ejaculation, and chronic pelvic pain are some conditions that can be linked with weak pelvic floor muscles.

Men

• Constipation or bowel strains
• Ongoing pain in your pelvic region, genitals or rectum.
• A prolapse – may feel as though there is a bulge/ pressure in the rectum or a feeling of needing to use your bowels without actually needing to go.
• Accidentally leaking urine when you exercise, laugh, cough or sneeze.
• Feelings of urgency in needing to the bathroom, or not making it there in time.
• Frequent need to urinate.
• Difficulty emptying your bladder (discontinuous urination – stop and start multiple times) and bowels.
• The feeling of needing to have several bowel movements during a short period of time.
• Accidentally passing wind.
• Pain in your lower back that cannot be explained by other causes.
• Pain in the testicles, penis (referred pain from the pelvic floor) or pelvis during intercourse.
• Erectile dysfunction.
• Painful ejaculation.
• Premature ejaculation.

Erectile function requires contraction of the pelvic floor muscles to block blood from leaving the penis. When the muscles are weak the outflow of blood from the penis is not stopped resulting in erectile dysfunction. Through learning voluntary control of the pelvic floor muscles this can help prevent premature ejaculation by learning how to relax and contract the muscles. Urinary incontinence has a direct relationship with pelvic floor muscles. These muscles tighten as a closure mechanism for the tube from the bladder to the exit (urethra) and weakness of these muscles can cause leaking and dribbling.

Women

• Pain or numbness during intercourse.
• Ongoing pain in your pelvic region, genitals or rectum.
• A prolapse – may be felt as a bulge in the vagina (feeling or seeing a bulge or lump in or coming out of your vagina) or a feeling of heaviness, discomfort, pulling, dragging or dropping sensation.
• Accidentally leaking urine when you exercise, laugh, cough or sneeze (stress incontinence).
• Feelings of urgency in needing to the bathroom, or not making it there in time.
• Frequent need to urinate.
• Difficulty emptying your bladder (discontinuous urination – stop and start multiple times) and bowels.
• The feeling of needing to have several bowel movements during a short period of time.
• Constipation or bowel strains.
• Accidentally passing wind.
• Pain in your lower back that cannot be explained by other causes.

Prolapse is a common condition that can occur due to weak pelvic floor muscles in women. This occurs due to the womb, bladder, bowel or top of the vagina moving out of their normal positions and pushing into the vagina. This can cause pain and discomfort but can be improved with pelvic floor exercises and lifestyle changes . Urinary incontinence has a direct relationship with pelvic floor muscles. These muscles tighten as a closure mechanism for the tube from the bladder to the exit (urethra) and weakness of these muscles can cause leaking and dribbling.

Diagnosis

It’s important not to self-diagnose your symptoms because they may indicate more serious conditions.

To make a diagnosis, your doctor will review your medical history and observe your symptoms. After the initial consultation, your doctor will perform a physical evaluation to check for muscle spasms or knots. They will also check for muscle weakness.

To check for pelvic muscle control and pelvic muscle contractions, your doctor may perform an internal exam by placing a perineometer — a small, sensing device — into your rectum or vagina.

A less invasive option involves placing electrodes on your perineum, the area between the scrotum and anus or vagina and anus, to determine if you can contract and relax pelvic muscles.

Risk Factors

The chances of developing pelvic floor dysfunction among men and women have increased over the past few years. According to Berghmans et al. (2015) this trend is likely to continue. The incidence of pelvic floor problems is predicted to increase by 35% between 2010-2030.

These statistics emphasize the importance of expanding knowledge related to the risk factors for pelvic floor dysfunction. When assessing a patient, physiotherapists should focus on a detailed subjective examination including past medical history and presenting condition/complaint, as this may reveal potential predispositions. Goal-centered conversations with the patients can provide guidance in planning treatment, and where applicable, liaising with appropriate healthcare professionals to ensure a holistic approach to care.

Men

• Prostate surgery: In general, scientific literature examining pelvic floor dysfunction among males is limited. However, prostate surgery has been identified as a potential risk factor . Specific pelvic floor disorders include urinary incontinence and erectile dysfunction, which are quite common post-operatively (up to 89% of men suffer from these conditions). Individuals who undergo this procedure may experience disturbance in pelvic floor muscles (especially urinary sphincters) and altered nerve supply to the area. In prostatectomy, the prostate (partially regulating continence) is removed, increasing the probability of incontinence. The urinary sphincter nerves may occasionally be damaged during surgery due to their proximity to the prostate. As a result, the patients might later experience poor bladder control. Cavernous nerves, which are responsible for erectile function, may also be disrupted.

Women

• Age: Females experiencing menopause are at increased risk for developing pelvic organ prolapse by 21.1%. Wu et al. (2014)assessed the relationship between age and number of pelvic floor disorders. They revealed that with each decade, the risk dramatically increased. This is most likely due to the hormonal fluctuations which change the functioning of female urogenital structures. It includes weakening of the pelvic floor, as the muscle mass tends to decrease during aging.
• Direct injury to levator ani (ex. vaginal delivery, fall on groin) and loss of tone in pelvic muscles: This involves the levator ani changing position and widening of genital hiatus, causing the pelvic structures to rely on the connective tissue for support. Over time, this alteration results in weakening or tearing of the tissue/collagen and may contribute to the occurrence of pelvic organ prolapse.
• Pregnancy and the nature of childbirth: Overstretching/damaging of the pudendal nerve during vaginal birth, prolonged labour, instrumental (forceps) delivery,episiotomy (surgical procedure to increase opening in vagina), weight and number of children (parity) have also been known to increase the pelvic floor dysfunction risk by 4-16%. These findings have been supported through biomechanical models of the pelvic floor. The researchers revealed that during the crowning of the fetal head in a vaginal birth, there is a greater risk for the avulsion of levator ani leading to a potential prolapse. Additionally, an episiotomy has been suggested to increase anal lacerations and therefore, incontinence risk. Findings within the systematic review noted parity to be a risk factor for primary pelvic organ prolapse as well.
• Genetics:Women who have a positive family history of pelvic organ prolapse, are more likely to inherit the condition. Campneau et al. (2011)showed that the risk for pelvic organ prolapse increased 1.4 times in the genetically predisposed group, after controlling for vaginal deliveries, hysterectomy, and incontinence. Additionally, some evidence suggests that in females who are experiencing urinary incontinence, the connective tissue of the pelvic floor muscles may be genetically weak. Low socioeconomic status: This factor, especially among racial minorities, may contribute to poorer access to adequate information regarding pelvic floor dysfunction. The lack of resources create a challenge in recognizing the symptoms and importance of seeking professional support in a timely manner. Hartigan and Smith (2018), presented that women of poorer socioeconomic status scored lower on the incontinence quiz than their higher socioeconomic status counterparts. Consequently, there is a strong emphasis on public education to reduce the risk of pelvic floor dysfunction. Hysterectomy (surgical removal of the uterus): This procedure often damages and weakens the pelvic muscles. Therefore, it may be a predisposing factor for pelvic organ prolapse . Lukanovic and Drazic (2010) suggest that that the incidence of postoperative complications after hysterectomy, including urinary and fecal incontinence was significantly higher in the group who undertook the surgery for vaginal prolapse compared to a control group with no diagnosis of prolapse. Being middle-aged, as an additional factor to post-hysterectomy, increases the risk to 60% for developing urinary incontinence.

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

TREATMENT-

The goal for treating pelvic floor dysfunction is to relax the pelvic floor muscles to make bowel movements easier and to provide more control.

Kegel exercises, or similar techniques that require you to contract your muscles, will not help this condition. While surgery is an option, there are less invasive treatment options available.

A common treatment for this condition is biofeedback. This technique allows your therapist to monitor how you relax or contract your pelvic muscles through special sensors. After observing your muscle activity, your therapist will tell you how to improve your coordination.

Other treatment options include:

• Medication. Your doctor may prescribe a muscle relaxant to help with pelvic floor dysfunction symptoms. The relaxants can prevent your muscles from contracting.
• Self-care. To reduce strain on your pelvic floor muscles, avoid pushing or straining when using the bathroom. Relaxation techniques such as yoga and stretching can also help to relax your pelvic floor muscles. Taking warm baths is another useful technique. Warm water improves blood circulation and relaxes the muscles.
• Surgery. If your pelvic floor dysfunction is the result of a rectal prolapse — a condition that causes the rectal tissue to fall into the anal opening — surgery will loosen the affected pelvic organs and cause them to relax.

Medical Management 

Pelvic floor dysfunction is a very treatable condition. Many ways exist to treat pelvic floor problems conservatively (non-surgical) and should generally be considered as the first-line option prior to more aggressive procedures such as surgery. Treatment will vary according to the nature of the condition or reason behind the dysfunction.

Pharmacological (Medication)

• Various drugs can be prescribed depending on the reason for the pelvic floor problems. Drug therapy is particularly common for urinary incontinence and will depend on the type of incontinence that your client is experiencing.
• The ageing process can lead to hormonal changes which can negatively impact the pelvic floor muscles and lead to increased laxity/stretching. Therefore, hormone replacement therapies for post-menopausal women can be used to manage or improve the symptoms.
• If your client has an over-active bladder or urge incontinence, there are medications to help relax the bladder and reduce the frequency of urination.
• Drug therapy is even more effective when used in combination with other strategies like pelvic floor exercises and lifestyle changes.

Surgical

• In some cases, when other strategies have been unsuccessful in achieving treatment goals, surgery may be the best treatment option. Depending on the specific condition, various procedures exist to address the problem.
• Incontinence and prolapse have multiple types of procedures to alter the pelvic structures or insert supports such as synthetic mesh slings, both in the goal of improving functions.
• For those who have a pelvic floor disorder, 1 in 9 will undergo surgery, however, there are risks associated with surgery as they don’t always succeed. Regarding synthetic mesh sling surgery, roughly 30% will require a second operation, and roughly 35% will need to be removed.
• Slightly less invasive options are also available, such as injections of Botox for urge incontinence or bulking agents to help reduce stress incontinence.

Physiotherapy Management

Education is the key and physiotherapists need to educate both male and female patients, on the function of the pelvic floor muscle. Assist the patient to understand the function of the pelvic floor muscle and how exercising this muscle can strengthen and reduce the risk of unwanted symptoms. This can help achieve that all important “buy in” and encourage the patient to be consistent with pelvic floor muscle training. However, explaining this can be tricky for any Physiotherapist due to the sensitivity of the subject! We have put together some tips that may be helpful to ensure a smooth, clear and lighthearted delivery!

• The Internal hammock – Try referring to the pelvic floor muscle as “ a hammock “ or a “trampoline “ which lies on the floor of the pelvis and supports organs such as the womb, bladder, bowel. This can make the function of the pelvic floor muscle easier to understand! And plus, who doesn’t want to learn about their very own internal trampoline, right?!
• Context is key! – Place emphasis on the strain that is put on the hammock or trampoline during everyday activities such as working, household duties, looking after family, exercising. Apply this to the patients’ life, by discussing their occupation, pastimes, and family situation and how the pelvic floor muscle or “trampoline “ is at risk of being overstretched as a result. This will help the patient to add context.
• Leaking waterworks?…. Time tighten up those taps! – Lack of bladder or bowel control can be a symptom of a weak pelvic floor and or a prolapse.This is an opportunity to empower the patient and show them they can still take control of their situation, through pelvic floor muscle training. Leaking, incontinence and increased urgency do not need to be tolerated! Ensure that the patient understands that there is an opportunity to tighten those taps right up! The only requirement is the right mindset and a top-notch spanner!
• Rome was not built in a day people! – It is important that physiotherapists stress that pelvic floor muscle training takes time, effort and consistency. Improvements in continence status and or stages of prolapse will not improve overnight and may take up to 3 weeks for any improvement to be felt. Be mindful of this and ensure that the patient is supported, as feelings of frustration may arise!
• If there is an issue, here is a tissue! – Physiotherapists deal with more than just muscles, we deal with emotions! It is important to be mindful of the impact that incontinence, leaking and prolapse can have on patient quality of life. Support, empathy, and compassion are an absolute necessity, to ensure the patient feels at ease. Listening to the patient and allowing them to tell you their concerns, hardships, and battles allow the patient to offload their worries and boost their feelings of self-efficacy as they begin their journey of self-management. Lending them your ear can be the greatest gift you can give.

The Correct Technique

Explaining a pelvic floor contraction is not an easy task! It is a difficult area, given the sensitivity of the subject that many patients feel uncomfortable with. Also, it is very confusing.  Medical and anatomical terminology can leave patients feeling lost or too embarrassed to ask questions. It is vital that exercising this complicated internal muscle is described in a simple but clear manner. Here are some tips that may be helpful, or if you find any nuggets of gold in this feel free to use!

The Female Contraction

• The pelvic floor muscle can be exercised in sitting standing or lying. Many patients seem to prefer sitting and feel the muscle is easier to engage in this position. Advise the patient to try out different positions to find what best suits
• In sitting, ensure both feet are placed on the floor and patient is relaxed and aware of their breathing. Encourage your patient to relax all muscles, including shoulders, abdominals, and glutes. Take a few moments to become aware of the breathing pattern.
• Ask the patient to imagine they are sitting on the toilet, having a wee. Ask them to then try and replicate the action of stopping the flow of urine mid-stream. Explain to them that this is a pelvic floor contraction involving the anterior muscles.
• Another handy example of a pelvic floor exercise is, again, ask the patient to imagine they are in a line waiting to pay for their shopping. They have been feeling bloated and the urge to pass wind has presented itself with full gusto! In order to hold that wind in it requires a contraction of the posterior pelvic floor muscles.
• Ask the patient to imagine they are sitting on the toilet. Ask them to then try and replicate the action of stopping the flow of urine mid-stream AND trying to stop themselves from passing wind at the same time. This involves a combined pelvic floor contraction of both anterior and posterior muscles.

Remember to remind your patients to never stop the flow of urine when actually going to the toilet as this may lead to difficulty in fully emptying the bladder in the long run! This is simply a visualization technique that may be helpful. Ensure to remind the patient that pelvic floor exercises can be done anytime anyplace, not only when sitting on the toilet!

EXERCISES-

The Knack Technique –   Get Involved People!

The knack technique can help to support pelvic floor health! Pressure builds up in the abdomen when lifting, exercising, coughing, sneezing laughing, lifting weights, turning to look out your rear window when driving. Basically, in pretty much everything we do! This creates a downward force or pressure on the pelvic floor muscles when can lead to our beloved internal “trampoline “ becoming stretched or laxThe knack technique involves contracting the pelvic floor muscle, before lifting, bending, sneezing, coughing, or any movement you can think of that will increase abdominal pressure. This is a supportive measure that can help maintain and support pelvic health.

The knack technique offers many benefits and can help patient’s become more involved in their pelvic health. Add context to this, go through patient activities of daily living, pastimes, family and suggest situations in which the knack technique can be useful. For example, lifting heavy shopping onto the kitchen counter, reminding the patient to contract the pelvic floor before lifting the bags, or contract the pelvic floor before lifting your 2-year-old teething toddler.

• Pelvic floor muscle training (PFMT) has been shown to be beneficial for both urinary incontinence and prolapse symptoms. A randomised control trial in adult women with pelvic floor dysfunctions suggests that using an intravaginal vibratory stimulus( IVVS) helps in improving the pelvic floor muscle strength as compared to intravaginal electrical stimulation (IVES). Findings from a review by Dumoulin et al. (2015) suggest that pelvic floor muscle training provides better outcomes compared to a control group in women with urinary incontinence. Li et al. (2016) found that those with pelvic organ prolapse undertaking pelvic floor muscle training had significantly greater improvements in subjective prolapse symptoms and objective prolapse severity compared to a control group.
• A study suggests that hypopressive exercises caused activation of the PFMs, abdominal, gluteal, and adductor muscles. 
• Pelvic floor training also seems to improve sexual function. The findings from a review by Ferreira et al. (2015) suggest that pelvic floor muscle training can improve sexual function or at least one sexual variable in women with pelvic floor dysfunction.
• Interesting findings from two RCTs also corroborate the evidence for pelvic floor muscle training. Alves et al. (2015) found that twelve group sessions of pelvic floor muscle training increased pelvic floor muscle contractility (p = 0.01) while decreasing urinary symptoms (p < 0.01) and anterior pelvic organ prolapse (p = 0.03). Hagen et al. (2014) found similar results with one to one sessions. They did note that longer-term investigations are required to strengthen the evidence.
• When prescribing a pelvic floor muscle training programme, adherence is important. According to a consensus statement by Dumoulin et al. (2015), a structured PFMT programme, an enthusiastic physiotherapist, audio prompts, use of established theories of behavior change, and user-consultations seem to increase adherence.
• The identified evidence fails to make any recommendations on the optimal dosage of pelvic floor muscle training.
• The NICE guidelines recommend a trial supervised PFMT programme for at least 3 months as first-line treatment for those with stress or urinary incontinence.At least 8 contractions three times a day.

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

INTRODUCTION –

Nutrition counseling is a cornerstone of prenatal care for all women during pregnancy. A woman’s nutritional status not only influences her health, but also pregnancy outcomes and the health of her fetus-neonate. Physicians and other healthcare providers need to be cognizant of nutritional needs during pregnancy, as they differ significantly compared to non-pregnant populations. Furthermore, an individualized approach to nutritional counseling that considers a woman’s access to food, socioeconomic status, race-ethnicity and cultural food choices, and body mass index (BMI) is recommended. In addition, many of the recommendations are geared for uncomplicated pregnancies, so adjustments need to be made when complications, such as gestational diabetes, arise. A nutritionist or registered dietitian can help facilitate dietary counseling and interventions. In this chapter, the maternal physiological adaptations as well as macronutrient and micronutrient requirements during pregnancy and lactation will be reviewed. Other discussions on these topics will include multiple gestations, obesity in pregnancy, pregnancies after bariatric surgery, special diets, and common exposures during pregnancy.

Nutrition and lifestyle before and during pregnancy, lactation, infancy and early childhood have been shown to induce long-term effects on later health of the child, including the risk of common non-communicable diseases such as obesity, diabetes and cardiovascular disease . This phenomenon is referred to as “Early metabolic programming of long-term health and disease” or “Developmental origins of adult health and disease”. The available evidence is based on experimental studies in animals, observations from retrospective and prospective observational studies in human cohorts, increasingly from controlled intervention trials. To strengthen the evidence base, researchers from 36 institutions across the European Union, the United States, and Australia collaborate in the European Commission funded “EarlyNutrition Research Project”. This international multidisciplinary research collaboration explores how nutrition and metabolism during sensitive time periods of early developmental plasticity can have an impact on cytogenesis, organogenesis, metabolic and endocrine responses as well as epigenetic modification of gene expression, thereby modulating later health. Because of the global escalation in the prevalence of obesity, particular focus has been placed on the developmental origins of adiposity (i.e., body fatness), leading to increasing evidence that early life programming could contribute to the intergenerational transmission of obesity and associated health outcomes. The EarlyNutrition Project has received funding from the European Commission (FP7-289346-EARLY NUTRITION), with co-funding provided by the Australian National Health and Medical Research Council (NMHMRC), and project partners to achieve a total budget of 11.1 million Euro. The project is co-ordinated by the Dr. von Hauner Children’s Hospital, LMU – Ludwig-Maximilians-Universität Munich, Germany. The project characterises programming effects and their effect sizes through studying contemporary prospective longitudinal cohort studies, performing randomized controlled intervention trials during pregnancy and infancy, and exploring underlying mechanisms. In order to facilitate translational application, the partnership reviewed available evidence and developed recommendations for dietary practice for women before and during pregnancy and lactation, and for infants and young children, taking long-term health consequences into account. These recommendations are devised for women and children in affluent countries, such as people in Europe.

Background: A considerable body of evidence accumulated especially during the last decade, demonstrating that early nutrition and lifestyle have long-term effects on later health and disease (“developmental or metabolic programming”). Methods: Researchers involved in the European Union funded international EarlyNutrition research project consolidated the scientific evidence base and existing recommendations to formulate consensus recommendations on nutrition and lifestyle before and during pregnancy, during infancy and early childhood that take long-term health impact into account. Systematic reviews were performed on published dietary guidelines, standards and recommendations, with special attention to long-term health consequences. In addition, systematic reviews of published systematic reviews on nutritional interventions or exposures in pregnancy and in infants and young children aged up to 3 years that describe effects on subsequent overweight, obesity and body composition were performed. Experts developed consensus recommendations incorporating the wide-ranging expertise from additional 33 stakeholders. Findings: Most current recommendations for pregnant women, particularly obese women, and for young children do not take long-term health consequences of early nutrition into account, although the available evidence for relevant consequences of lifestyle, diet and growth patterns in early life on later health and disease risk is strong. Interpretation: We present updated recommendations for optimized nutrition before and during pregnancy, during lactation, infancy and toddlerhood, with special reference to later health outcomes. These recommendations are developed for affluent populations, such as women and children in Europe, and should contribute to the primary prevention of obesity and associated non-communicable diseases.

Improving Nutrition and Health for Pregnant and Lactating Women-

Maternal nutrition-

Nutrition for women in pre-pregnancy, pregnancy, and over the first two years of the child’s life is of utmost importance for the survival, health and development of mothers and their children. In pregnancy, requirements of energy, protein, and essential micronutrients (vitamins and minerals) are increased not only to maintain the mother’s own health, but to also support optimal physical and brain development in the foetus. Furthermore, nutrition reserves are built over pregnancy to produce breastmilk for the post-child birth phase. Deficiencies of energy, protein, iron, calcium, iodine, vitamin A and folic acid during pregnancy predispose mothers to maternal complications and even mortality. These also contribute to foetal birth defects, low birth weight, restricted physical and mental potential, and foetal or newborn mortality.

Exclusive breastfeeding is recommended for infants 0-6 months of age to meet all their nutrition needs for optimal growth, and to protect them from infection. This should be followed by continued breastfeeding alongside appropriate complementary feeding until the child reaches 2 years of age. To sustain the production of adequate quantity and nutritional quality of breastmilk, lactating women have higher requirements of energy, protein, and other micronutrients. Poor maternal nutrition over this period risks depletion of the mother’s own nutrient stores and health, and harms the nutrition and health of the growing child . Addressing nutritional needs of pregnant and lactating women is now entrenched within the Sustainable Development Goals. By scaling up efforts to achieve this target, progress will also be accelerated on the targets on maternal and child mortality and health.

Maternal nutrition and health-

The impact of poor nutrition on maternal health and survival is indisputable. Anaemia, which results from deficiencies of nutrients such as iron and folic acid is an important risk factor for haemorrhage; a leading cause of maternal mortality. Calcium deficiency during pregnancy also increases the risk of pre-eclampsia, another cause of maternal mortality . Improving nutrition alongside good antenatal care can reduce these numbers significantly. Globally 52% of maternal deaths are attributable to haemorrhage, sepsis, and hypertensive disorders; 28% to non-obstetric causes; 8% to unsafe abortion . Infection during pregnancy can deteriorate a mother’s nutritional and health status, and impact foetal development. Maternal infections before or during childbirth are known to be associated with around 1 million new-born deaths each year, and contribute to about 10% of the global burden of maternal mortality. Malnutrition, is one of the main factors increasing the risk of such life-threatening infections through its role in decreasing immunity and delaying recovery .

PREGNANCY

Energy Expenditure during Pregnancy

Caloric intake should increase by approximately 300 kcal/day during pregnancy. This value is derived from an estimate of 80,000 kcal needed to support a full-term pregnancy and accounts not only for increased maternal and fetal metabolism but for fetal and placental growth. Dividing the gross energy cost by the mean pregnancy duration (250 days after the first month) yields the 300 kcal/day estimate for the entire pregnancy. However, energy requirements are generally the same as non-pregnant women in the first trimester and then increase in the second trimester, estimated at 340 kcal and 452 kcal per day in the second and third trimesters, respectively. Furthermore, energy requirements vary significantly depending on a woman’s age, BMI, and activity level. Caloric intake should therefore be individualized based on these factors.

Laboratory Testing during Pregnancy

Physiological changes during pregnancy alter the normal ranges of several laboratory values. Both total red blood cell mass and plasma volume increase, but plasma volume increases to a greater extent resulting in hemodilution and anemia during pregnancy. Consequently, a hemoglobin <10.5 g/dl or a hematocrit <32% is considered anemic during the second trimeste. Serum total protein and albumin also decrease by approximately 30% compared to non-pregnant values. Additionally, because estrogen increases the hepatic production of certain proteins, there is greater protein binding of corticosteroids, sex steroids, thyroid hormones, and vitamin D during pregnancy, resulting in lower free levels.

Nutrients

Macronutrients

Recommended protein intake during pregnancy is 60g/day, which represents an increase from 46g/d in non-pregnant states. In other words, this increase reflects a change to 1.1g of protein/kg/day during pregnancy from 0.8g of protein/kg/day for non-pregnant states. Carbohydrates should comprise 45-64% of daily calories and this includes approximately 6-9 servings of whole grain daily. Total fat intake should comprise 20-35% of daily calories, similar to non-pregnant women.

Micronutrients

The recommendations for daily micronutrient intake for a pregnant woman are determined by the “Recommended Dietary Allowances” or RDA data. In general, these RDA refer to the levels of intake of essential nutrients that are judged by the Food and Nutrition Board of the Institute of Medicine (IOM) to be adequate to meet the known nutrient needs of practically all healthy persons. The RDA have been modified for pregnant women. shows the dietary allowances for most vitamins and minerals during pregnancy and they are reviewed in further detail below.

A daily prenatal multivitamin is generally recommended before conception and during pregnancy. describes the typical composition of a prenatal vitamin. The critical difference compared to other multivitamins is the folic acid dose, which is necessary to support rapid cell growth, cell replication, cell division, and nucleotide synthesis for fetal and placental development. While there is data to support additional folic acid and iron supplementation during pregnancy, there is no high quality evidence demonstrating that all women require the increased levels of nutrients in a prenatal vitamin.

Gestational Weight Gain

Pregnancy has traditionally been considered a time for weight gain, not weight loss. The obligatory weight gain during pregnancy is approximately 8 kg which accounts for the fetus, the placenta, amniotic fluid volume, and adaptations to maternal tissues (e.g., uterus, breast, blood volume). A weight gain less than this amount implies that existing maternal adipose and protein stores would be mobilized in order to support the pregnancy. Metabolic changes of women who lose weight during pregnancy are not well-described, but ketonemia, increased urinary nitrogen excretion, and decreased gluconeogenic amino acid production result after a period of fasting during pregnancy. Pregnancy is often considered a time of “accelerated starvation” due to the increase in insulin resistance, with an increased risk for developing ketonuria and ketonemia. This physiologic change is important to consider in the setting of weight loss during pregnancy because maternal ketonemia or ketonuria may subsequently be associated with abnormal fetal growth or later neurocognitive developmen.

Obesity

The World Health Organization and the National Institutes of Health define normal weight as a BMI of 18.5–24.9 kg/m², overweight as a BMI of 25–29.9 kg/m², and obesity as a BMI of 30 kg/m² or greater. Obesity is further categorized by BMI into Class I (30–34.9 kg/m²), Class II (35–39.9 kg/m²), and Class III or extreme obesity (≥ 40 kg/m²).Trends in adult weight over the past couple of decades highlight the escalating role that obesity plays in women’s health; 31.8% of reproductive age women (20-39 years) had obesity in 2011-2012.Women with a higher pre-pregnancy BMI have a greater risk for adverse perinatal outcomes. These include both maternal complications such as gestational diabetes, pregnancy-related hypertension, and cesarean deliveries along with adverse fetal effects such as birth defects, stillbirth, and abnormal fetal growth.As such, weight loss prior to pregnancy is strongly recommended in order to reduce the risk of these complications.

Pregnancy after bariatric surgery

Pregnancy after bariatric surgery is not uncommon as fertility often improves after a bariatric surgery procedure.Given that bariatric procedures can create deficiencies of micro- and macronutrients, a pregnancy occurring after a bariatric surgery procedure requires particular attention to nutritional status. As stated previously, requirements for calories, vitamins, and minerals increase during pregnancy, so nutritional deficiencies in the bariatric surgery patient can be exacerbated during pregnancy. The most common deficiencies that occur after bariatric surgery are vitamin B₁₂, folate, and iron.Because malabsorptive procedures (e.g., Roux-en-y gastric bypass [RYGB], biliopancreatic diversion) have a higher risk for nutritional deficiencies, closer surveillance in pregnancies that occur after these types of surgeries is appropriate. However, derangements in nutrients can also occur after restrictive-type procedures (e.g., laparoscopic adjustable gastric banding), so it may be reasonable to screen all women who are pregnant post-bariatric surgery for nutritional deficiencies. Guidelines for screening and management of nutritional deficiencies during pregnancy are adapted from those designed for non-pregnant states and include laboratory testing once a trimester or every 3 months if the levels are normal .Iron deficiency anemia is frequently a long-term complication of bariatric surgery, occurring in 6% to 50% of patients after RYGB. In pregnancies after bariatric surgery, iron deficiency anemia can be diagnosed in the usual manner with a low mean corpuscular volume, and abnormal iron studies (e.g., low serum iron, high total iron-binding capacity, and a low serum ferritin) keeping in mind the physiologic anemia that occurs during pregnancy . Treatment of vitamin and mineral deficiencies during pregnancy, in terms of dose and duration, is similar to that of non-pregnant states.

Vegetarians

There are varying types of vegetarian diets such as ovolactovegetarian (includes dairy and egg products), ovovegetarian (includes eggs), lactovegetarian (includes dairy products), and vegan (excludes eggs, dairy, and any other animal products). Alternative protein sources for these women include beans, peas, soy, nuts, nut butter, and milk and egg products. Minerals that may be deficient in their diets include iron, calcium, zinc, and vitamin B₁₂. Laboratory testing for these specific nutrients may be indicated.

Eating disorders

For women with either a history of or current eating disorder (e.g., anorexia nervosa, bulimia), additional questions regarding their weight should be asked including how they feel about weight gain, being weighed at every prenatal visit (which is customary in prenatal care practices in the United States), and the ongoing changes in their body.With respect to weighing, a woman’s preference about weighing (i.e., whether or not she prefers to see the numbers) should be assessed and documented in the chart. Counseling on gestational weight gain goals is still important for these women as weight influences the growth and development of the fetus. Similar to management prior to pregnancy, a collaborative team of experts in eating disorders should continue to manage and treat these women during the pregnancy.

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

LACTATION

Physiology and Production

Breastfeeding and breast milk are the global standard for infant feeding. The World Health Organization, the U.S. Surgeon General, the American Academy of Pediatrics, the American Congress of Obstetricians and Gynecologists, the American Academy of Family Practice, and the Academy of Breastfeeding Medicine all support this statement. The American Academy of Pediatrics further recommends exclusive breastfeeding for the first 6 months and breastfeeding at least through the first year of life.Similar to pregnancy, energy and nutritional requirements also differ during lactation and breastfeeding.

Women who breastfeed require approximately 500 additional kcal/day beyond what is recommended for non-pregnant women.The estimate is derived from the mean volume of breast milk produced per day (mean 780 mL, range 450-1200 mL) and the energy content of milk (67 kcal/100 mL).During pregnancy, most women store an extra 2 to 5 kg (19,000 to 48,000 kcal) in tissue, mainly as fat, in physiologic preparation for lactation. If women do not consume the extra calories, then body stores are used to maintain lactation. It is not unusual for lactating women to lose 0.5-1.0 kg/month after the first postpartum month.

Special Considerations

Multiple Gestations

Approximately 40-90% of mothers of twins initiate breastfeeding.⁸⁷ The production of milk is primarily determined by infant demand rather than the maternal capacity to lactate. As such, for women attempting to breastfeed twins and triplets, the supply will meet the demand. Continuation of micronutrient supplementations given antenatally in the form of a prenatal vitamin is appropriate for women who are breastfeeding twins. Twins can breastfeed either simultaneously or separately.

Special Considerations

Multiple Gestations

Approximately 40-90% of mothers of twins initiate breastfeeding.The production of milk is primarily determined by infant demand rather than the maternal capacity to lactate. As such, for women attempting to breastfeed twins and triplets, the supply will meet the demand. Continuation of micronutrient supplementations given antenatally in the form of a prenatal vitamin is appropriate for women who are breastfeeding twins. Twins can breastfeed either simultaneously or separately.

Approximately 40-90% of mothers of twins initiate breastfeeding. The production of milk is primarily determined by infant demand rather than the maternal capacity to lactate. As such, for women attempting to breastfeed twins and triplets, the supply will meet the demand. Continuation of micronutrient supplementations given antenatally in the form of a prenatal vitamin is appropriate for women who are breastfeeding twins. Twins can breastfeed either simultaneously or separately.

Obesity

Several studies have demonstrated that women with obesity have decreased rates of initiating breastfeeding and breastfeed for shorter durations compared to normal weight women.Biological (i.e. delayed lactation), psychological (i.e., embarrassment related to body size and difficulty in breastfeeding discreetly), mechanical (i.e., larger breasts and nipples that create difficulties with latching), and medical (i.e., cesarean deliveries, diabetes, thyroid dysfunction) factors have been theorized to explain these findings, but the exact etiology is likely a combination of factors. To combat this trend and increase the likelihood that women with obesity attain their breastfeeding goals, they need additional support and encouragement to breastfeed, including assistance with appropriate latching techniques and demonstration of appropriate infant positions, to aid with initiation and continuation of lactation.

Bariatric surgery

Women who have had bariatric surgery are also advised to follow the recommendation of breastfeeding for at least 6 months. Laboratory evaluation of micronutrient levels, as described in for pregnant women, is also recommended for breastfeeding women after bariatric surgery, with one group suggesting they be tested as frequently as every 3 months. The infant’s provider also should be aware of the mother’s history of bariatric surgery as well as any of her specific dietary restrictions or identified nutrient deficiencies. For women who have a gastric banding procedure, one recommendation is to keep the band deflated until the successful establishment of breastfeeding. Though few studies have evaluated the nutritional content of breast milk produced by lactating women after bariatric surgery, it is likely similar to other women. While infants who are born to women with obesity have a higher rate of early childhood obesity, this may be offset by the reduced risk of early childhood obesity in infants who are predominantly breastfed.

Vegetarians

Recommended dietary guidelines for vegetarians during lactation are lacking. Vitamin D supplements are recommended for women who do not drink milk or other food fortified with vitamin D. A vitamin B₁₂ supplement (2.6 μg/d) is also recommended for women who consume ovolactovegetarian and vegan diets. Another recommendation is to consume 1200-1500 mg/day of calcium because of the possible decreased intake and absorption from a plant-based diet.The FDA recommends similar precautions regarding avoiding higher mercury fish during lactation. Adverse neonatal effects have not been demonstrated with ordinary maternal fish consumption during breastfeeding.

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

INTRODUCTION-

An abscess in the brain of an otherwise healthy person is usually caused by bacterial infection. Fungal brain abscesses tend to occur in people with weakened immune systems. The infection will cause your brain to swell from the collection of pus and dead cells that forms.

A brain abscess forms when fungi, viruses, or bacteria reach your brain through a wound in your head or an infection somewhere else in your body. According to the Children’s Hospital of Wisconsin, infections from other parts of the body account for between 20 and 50 percent of all brain abscess cases. Heart and lung infections are among the most common causes of brain abscesses. However, brain abscesses can also begin from an ear or sinus infection, or even an abscessed tooth.

See your doctor right away if you think you may have a brain abscess. You’ll need the appropriate treatment to prevent any brain damage from the swelling.

Intracranial abscesses are uncommon, serious, life-threatening infections. They include brain abscess and subdural or extradural empyema and are classified according to the anatomical location or the etiologic agent. The term brain abscess is used in this article to represent all types of intracranial abscesses.

Intracranial abscesses can originate from infection of contiguous structures (eg, otitis media, dental infection, mastoiditis, sinusitis) secondary to hematogenous spread from a remote site (especially in patients with cyanotic congenital heart disease), after skull trauma or surgery, and, rarely, following meningitis. In at least 15% of cases, no source can be identified.

A brain abscess is a collection of pus that develops in response to an infection or trauma. It remains a serious and potentially life-threatening condition.

In the past, a brain abscess was “invariably fatal,” but researchers writing in 2014 noted that progress in diagnosis and treatment have significantly increased the chances of survival.

The effects vary, depending on the size of the abscess and where it forms in the brain.

Between 1,500 and 2,500 cases occur each year in the United States. Brain abscesses are most likely to affect adult men aged under 30 years. Among children, they most commonly develop in those aged 4–7 years. Newborns are also at risk.

Vaccination programs have reduced the incidence of brain abscesses in young children.

CAUSES-

A brain abscess is most likely to result from a bacterial or fungal infection in some part of the brain. Parasites can also cause an abscess.

When the bacteria, fungi, or parasites infect part of the brain, inflammation and swelling occur. In these cases, the abscess will consist of infected brain cells, active and dead white blood cells, and the organisms that cause the problem.

As the cells accumulate, a wall or membrane develops around the abscess. This helps to isolate the infection and keep it from spreading to healthy tissue.

If an abscess swells, it puts increasing pressure on surrounding brain tissue.

The skull is not flexible, and it cannot expand. The pressure from the abscess can block blood vessels, preventing oxygen from reaching the brain, and this results in damage or destruction of delicate brain tissue.

here are 3 main ways a brain abscess can develop. These are:

• an infection in another part of the skull – such as an ear infection, sinusitis or dental abscess, which can spread directly into the brain
• an infection in another part of the body – for example, the infection that causes pneumonia spreading into the brain via the blood
• trauma, such as a severe head injury – that cracks open the skull, allowing bacteria or fungi to enter the brain

However, in some cases, the source of the infection remains unknown.

SYMPTOM-

Symptoms usually develop slowly over several weeks, but they can also come on suddenly. Symptoms you should watch for are:

• differences in mental processes, such as increased confusion, decreased responsiveness, and irritability
• decreased speech
• decreased sensation
• decreased movement due to loss of muscle function
• changes in vision
• changes in personality or behavior
• vomiting
• fever
• chills
• neck stiffness, especially when it occurs with fevers and chills
• sensitivity to light

In babies and young children, most of the symptoms are similar. However, your child may show other symptoms of a brain abscess. The soft spot on top of your baby’s head, called the fontanelle, may be swollen or bulging. Other symptoms in your child can include:

• projectile vomiting
• high-pitched crying
• spasticity in the limbs

The signs and symptoms of a brain abscess are as follows:

• a headache (69–70 percent of cases)
• a fever (45–53 percent)
• seizures (25–35 percent)
• nausea and vomiting (40 percent)

A seizure may be the first sign of an abscess. Nausea and vomiting tend to occur as pressure builds inside the brain.

Pain usually starts on the side of the abscess, and it may begin slowly or suddenly.

Changes in mental status occur in 65 percent of cases, and they may lead to:

• confusion
• drowsiness and lethargy
• irritability
• poor mental focus
• poor responsiveness
• slow thought processes
• coma (possibly)

Neurologic difficulties affect 50–65 percent of people with brain abscesses. These issues often follow a headache, appearing within days or weeks, and they can include:

• muscle weakness
• weakness or paralysis on one side of the body
• speech problems, such as slurred speech
• poor coordination

Other symptoms may include:

• a stiff neck, back, or shoulders
• blurred, double, or graying vision

The symptoms of a brain abscess result from a combination of infection, brain tissue damage, and pressure on the brain, as the abscess grows to take up more space.

If the headache suddenly becomes worse, it may mean that the abscess has burst.

In two-thirds of cases, symptoms are present for as long as 2 weeks. On average, doctors diagnose the issue 8 days after symptoms start.

When to get medical advice

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

Any symptoms that suggest a problem with the brain and nervous system should be treated as a medical emergency. These include:

• slurred speech
• muscle weakness or paralysis
• seizures occurring in a person with no previous history of seizures

If you or someone you know experiences any of these symptoms, phone 999 immediately and ask for an ambulance.

Any symptoms that suggest a worsening infection, such as a high temperature or being sick, should be reported to your GP immediately.

DIAGNOSIS-

Many of these symptoms closely resemble other diseases or health problems. Talk to your doctor immediately if you develop any of the symptoms. You’ll likely need a neurological exam. This exam can reveal any increased pressure within the brain, which can occur from swelling. CT and MRI scans can also be used to diagnose a brain abscess.

In some cases, your doctor may need to perform a lumbar puncture, or spinal tap. This involves the removal of a small amount of cerebral spinal fluid to test for any problems other than an infection. A lumbar puncture will not be performed if any significant brain swelling is suspected, as it can temporarily worsen the pressure inside the head. This is to avoid the risk of brain hematoma, or a ruptured blood vessel in the brain.

To diagnose a brain abscess, the doctor will evaluate signs and symptoms and look at the patient’s recent medical and travel histories.

They will need to know whether the individual:

• has had an infection recently
• has a weakened immune system

Symptoms can be similar to those of other illnesses and conditions, so it may take time to confirm a diagnosis. The diagnosis will be more straightforward if the doctor can pinpoint exactly when symptoms started and how they progressed.

Tests may include:

• a blood test to check for high levels of white blood cells, which can indicate an infection
• imaging scans, such as an MRI or a CT scan, in which an abscess will show up as one or more spots
• a CT-guided aspiration, a type of needle biopsy, which involves taking a sample of pus for analysis

The number of fatalities from brain abscesses has fallen in recent decades, due to the increasingly routine use of CT and MRI scans in detection.

How infection enters the brain

Brain infections are fairly uncommon for several reasons.

One reason involves the blood-brain barrier, a protective network of blood vessels and cells. It blocks certain components from the blood that flows to the brain, but it allows others to pass through.

Sometimes, an infection can get through the blood-brain barrier. This can happen when inflammation damages the barrier, leading to gaps.

The infection enters the brain through three main routes.

It may:

• come through the blood from an infection in another part of the body
• spread from a nearby site, such as the ear
• result from a traumatic injury or surgery

Infection from another area of the body

If an infection occurs somewhere else in the body, the infectious organisms can travel through the bloodstream, bypass the blood-brain barrier, and enter and infect the brain.

Between 9 and 43 percent of abscesses result from pathogens that traveled from another part of the body.

Many bacterial brain abscesses stem from a lesion somewhere else in the body. It is crucial to find that primary lesion, or there may be a repeat infection in the future.

A person with a weakened immune system has a higher risk of developing a brain abscess from a bloodborne infection.

A person may have a weakened immune system if they:

• have HIV
• have AIDS
• are infants under the age of 6 months
• are receiving chemotherapy
• are using long-term steroid medication
• have had an organ transplant and take immunosuppressant drugs to prevent organ rejection

The most common infections known to cause brain abscesses are:

• endocarditis, an infection of the heart valve
• pneumonia, bronchiectasis, and other lung infections and conditions
• abdominal infections, such as peritonitis, an inflammation of the inner wall of the abdomen and pelvis
• cystitis, or inflammation of the bladder, and other pelvic infections

Direct contagion-

An infection can spread from a nearby area, and this accounts for 14–58 percent of brain abscesses.

If an infection starts inside the skull, for example in the nose or the ear, it can spread to the brain.

Infections that can trigger a brain abscess include:

• otitis media, or a middle ear infection
• sinusitis
• mastoiditis, an infection of the bone behind the ear

The location of the abscess may depend on the site and type of the original infection.

Direct trauma

A brain abscess can result from trauma, such as from neurological surgery or a penetrating brain injury.

An abscess can result from:

• a blow to the head that causes a compound skull fracture, in which fragments of bone are pushed into the brain
• the presence of a foreign body, such as a bullet, if someone does not remove it
• a complication of surgery, in rare cases

What are the risk factors?

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com

Nearly anyone can get a brain abscess, but certain groups of people are at a higher risk than others. Some diseases, disorders, and conditions that raise your risk include:

• a compromised immune system due to HIV or AIDS
• cancer and other chronic illnesses
• congenital heart disease
• major head injury or skull fracture
• meningitis
• immunosuppressant drugs, such as those used in chemotherapy
• chronic sinus or middle ear infections

Certain birth defects allow infections to reach the brain more easily through the teeth and intestines. One example of this is tetralogy of Fallot, which is a heart defect.

TREATMENT-

Treatment for a brain abscess usually involves a combination of medicines and surgery, depending on the size and number of brain abscesses.

A brain abscess is a medical emergency, so you’ll need treatment in hospital until your condition is stable.

Treatment with medicines often begins before a diagnosis is confirmed to reduce the risk of complications.

Medicines

In some cases, it may be possible to treat an abscess with medicine alone, or surgery may be too risky.

Medicines are recommended over surgery if you have:

• several abscesses
• a small abscess (less than 2cm)
• an abscess deep inside the brain
• meningitis (an infection of the protective membranes that surround the brain) as well as an abscess
• hydrocephalus (a build-up of fluid on the brain)

You’ll normally be given antibiotics or antifungal medicine through a drip, directly into a vein. Doctors will aim to treat the abscess and the original infection that caused it.

Surgery

If the abscess is larger than 2cm, it’s usually necessary to drain the pus out of the abscess. However, you’ll still need a course of antibiotics after surgery.

There are 2 surgical techniques for treating a brain abscess:

• simple aspiration
• craniotomy

Simple aspiration involves using a CT scan to locate the abscess and then drilling a small hole known as a “burr hole” into the skull. The pus is drained and the hole sealed.

A simple aspiration takes around an hour to complete.

Open aspiration and excisions are usually carried out using a surgical procedure known as a craniotomy.

Craniotomy

A craniotomy may be recommended if an abscess does not respond to aspiration or reoccurs at a later date.

During a craniotomy, the surgeon shaves a small section of your hair and removes a small piece of your skull bone (a bone flap) to gain access to your brain.

The abscess is then drained of pus or totally removed. CT-guidance may be used during the operation, to allow the surgeon to more accurately locate the exact position of the abscess.

Once the abscess has been treated, the bone is replaced. The operation usually takes around 3 hours, which includes recovery from general anaesthetic, where you’re put to sleep.

Complications of a craniotomy

As with all surgery, a craniotomy carries risks, but serious complications are uncommon.

Possible complications of a craniotomy may include: 

• swelling and bruising around your face – which is common after a craniotomy and should lessen after the operation
• headaches – these are common after a craniotomy and may last several months, but should eventually settle down
• a blood clot in the brain – further surgery may be required to remove it
• stiff jaw – the surgeon may need to make a small cut to a muscle that helps with chewing, which will heal but can become stiff for a few months; exercising the muscle by regularly chewing sugar-free gum should help relieve the stiffness
• movement of the bone flap – the bone flap in your skull may feel like it moves and you may experience a clicking sensation; this can feel strange, but it is not dangerous and will stop as the skull heals

The site of the cut (incision) in your skull can become infected, although this is uncommon. You’re usually given antibiotics around the time of your operation to prevent infection.

Recovering from surgery

Once your brain abscess has been treated, you’ll probably stay in hospital for several weeks so your body can be supported while you recover.

You’ll also receive a number of CT scans, to make sure the brain abscess has been completely removed.

Most people need a further 6 to 12 weeks rest at home before they’re fit enough to return to work or full-time education.

After treatment for a brain abscess, avoid any contact sport where there’s a risk of injury to the skull, such as boxing, rugby or football.

Advice for drivers

If you’ve had brain surgery and you hold a driving licence, you’re legally required to inform the Driver & Vehicle Licensing Agency (DVLA).

It’s likely that the DVLA will suspend your driving licence due to your increased risk of having a seizure. Your licence will only be returned once your GP or surgeon confirms it’s safe for you to drive.

For most people, this is likely to be 12 months after surgery without having any seizures during this time.

REQUEST AN APPOINTMENT OR BOOK A CONSULANT – Sargam.dange.18@gmail.com