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Review Article Indian Pediatrics 2006; 43:409-415 |
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Emergency and Intensive Care Management of a Comatose Patient with Intracranial Hypertension: Current Concepts |
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Suchitra Ranjit Correspondence to: Dr S. Ranjit, Consultant
Pediatric Intensivist, Apollo Hospitals, Chennai, India.
This article attempts to guide the pediatrician through a problem oriented, prioritized approach to a child presenting with coma in the Emergency Room and Intensive Care, stressing the importance of early stabilization of the vitals, including early controlled ventilation. The dangers of overzealous hyperventilation, early lumbar puncture as well as the basis for the current recommendations for fluid therapy in modern neuro-critical care are discussed. Many algorithms in standard western literature are based on continuous intracranial pressure (ICP) measurement, a monitoring modality that is not widely available in India. The following guidelines outline ten steps of empiric ICP management, an approach that may have limitations of significant over and under treatment with attendant complications. Guidelines for differentiating causes of coma are shown in Table I(1-9) Table I Causes of Coma (TIPS from VOWELS)(1,9)
Important causes of coma in Indian children include bacterial, tuberculous and viral meningoencephalitis, malaria; non-infectious causes including stroke, ingestions and Reye syndrome(2-8).
Management goals The main goals of care include optimizing cerebral blood flow (CBF)/ cerebral perfusion pressure (CPP) and minimizing factors that can aggravate neuronal injury or trigger intra-cranial pressure (ICP) elevation(9-12). 1. Assess the Airway, Breathing and Circulation (ABCs) The airway should be stabilized and an assessment made for the need for intubation. Even if spontaneously breathing with normal gas exchange, many comatose children will benefit from intubation, especially if they have intracranial hypertension(9,11). Early intubation, ventilation and deep sedation are often overlooked as key interventions for ICP control(10). A GCS below 8 has been the standard indication for intubation. Recent literature however states that intubation should be considered in patients with a GCS below 12(11). Other indications for intubation include deterioration in the level of conscious-ness, evidence of herniation and irregularities in respiration (Table II)(9-11). Table II Signs of cerebral herniation(9-11)
* (Cushings Triad) - Late findings
The blood pressure should be kept at the higher range of normal (for age). This requires ensuring appropriate fluid and inotrope management(10,11). 2. Assess and Treat for Immediately Correctable Cause of Coma Perform bedside capillary glucose test and correct if low, send samples to lab for routine hematological and biochemical testing. 3. Assessment of the Depth of Coma The standard assessment tool is the Glasgow Coma Score (GCS) in older children and modified GCS in children <5 years old(1,2,13). The AVPU score A (Awake), V (Response to verbal commands), P (Response only to pain), U (unresponsive) is an alternate coma score(1). 4. Assessment and Treatment of Raised ICP The focus of contempory ICP management has changed in recent years in two important aspects: firstly, increasing emphasis on CPP (cerebral perfusion pressure) management in addition to ICP control and secondly, the increasing recognition of the potential for overzealous hyperventilation to aggravate cerebral ischemia by reducing CBF(9-12). CPP = Mean arterial pressure (MAP) – Intracranial pressure (ICP) Cerebral ischemia may result when CPP is lowered, either from raised ICP or lowered MAP (hypotension). When the ICP is critically raised, herniation syndromes (uncal, central or medullary herniation) can occur, which, along with hypoxic-ischemic damage from reduced CPP, are the most important causes of death(10,11). Table III describes the signs of herniation(9,11). Table III Mannitol: Concerns and contra-indications(10,11,17)
*Emergency therapy for herniation syndromes: 1.0-1.5 g/kg of 20% mannitol, Subsequent doses: 0.2.5-0.5 g/kg Q4-6H, measure serum osmolality If raised ICP is clinically suspected, therapeutic measures should be immediately instituted as papilledema may not be seen in acutely elevated ICP and fatal herniation can occur even after a "normal" CT scan(11,14). Role of Mannitol Mannitol is indicated acutely for patients in whom there is a strong clinical suspicion of raised ICP or imminent herniation(9-11). Mannitol has two distinct effects(9,10,15). The immediate effect is related to its rheologic properties (decreased blood viscosity) resulting in a transient increased CBF followed by a more sustained fall in CBF. The delayed osmotic effects occur after 15-30 minutes and last for 4-6 hours. Urinary fluid losses should be replaced with normal saline to avoid volume depletion(10). Emerging Role of Hypertonic Saline (HTS) (16-21) HTS acts like mannitol by establishing a constant osmolar gradient in order to draw fluid from the brain parenchyma but without the risks of dehydration and tubular damage as in the case of mannitol. In the hypotensive/hypoperfused patient, HTS may be the osmotherapy of choice for reducing ICP while maintaining MAP/CPP, although most literature is this context is in reference to adults(16,17). However, beneficial effects of HTS with a low frequency of side-effects have been described in the setting of pediatric traumatic brain injury(18,19) and cerebral edema occurring during DKA treatment in children(20-21). 5. Anti-seizure Medications in Coma Convulsions can cause massive increases in CBF , consequent increase in ICP, can lead to secondary brain damage and may precipitate or be precipitated by cerebral herniation(9-12). Apart from generalized tonic clonic seizures (GTCS), some comatose children may have non-convulsive seizures (NCS) manifesting with subtle signs such as eyelid twitching, eye deviation or nystagmus(11). A bedside EEG may be informative(22). If in doubt, empiric treatment of seizures may be justified and can result in improvement of consciousness(11). 6. Neuro-imaging Urgent imaging is indicated in afebrile coma and the presence of focal signs or papilledema, as the diagnosis includes stroke, intra-cranial bleed, tumor or hydro-cephalus(11,22). However, any child who does not have a very obvious metabolic/ toxic cause for the coma generally requires to be imaged. A CT scan may provide information about the cause of altered mental status and the presence of intracranial hypertension(22), however a normal CT scan does not rule out raised ICP(11). An MRI may be more specific for early changes of herpes simplex encephalitis (where CT may be normal), posterior fossa and white matter pathology(9,11) . A cranial ultrasound may miss subdural collections or even extensive infarcts and a CT or MRI is an essential investigation in a deeply comatose infant even when the anterior fontanelle is open(11). 7. Lumbar Puncture (LP) in a Comatose Child The potential benefits of early LP include making an early diagnosis of CNS infection and identification of the pathogen and drug sensitivities(9,23). Contra-indications for LP include signs of cerebral herniation, low GCS, focal neurological signs, or cardiorespiratory compromise(9,11,23). In an unconscious child with potential raised ICP , the decision is controversial with some authors stating that the risk of herniation far outweighs the benefit of knowing the pathogen from an early LP(24). 8. Choice of Empiric Antimicrobials If a CNS infection is suspected in a febrile child presenting in acute coma and seizures, empiric anti-microbial should include acyclovir in addition to a third generation cephalosporin until further confirmatory tests are available(11). The need for empiric anti-malarials should be carefully assessed(6,11). 9. Fluid Therapy There is accumulating data that hypovolemia worsens outcome in children with meningitis(25-27), malaria(28) and severe head injury(18,19). Hypovolemia (fluid restriction, diuretics) can lower the CPP and lead to worse ICP due to auto-regulatory vasodilation(10) .What must be restricted are hypotonic fluids such as 1/5th normal saline in 5% dextrose (Isolyte P). The dextrose will be metabolized with a resultant hypotonic fluid that can exacerbate cerebral edema and ICP(10-12). Adult and pediatric literature stress the importance of avoiding both hyperglycemia as well as hypoglycemia since the former can also worsen neurological out-come(10,18,19,29) . Enteral feeds should be started at the earliest(11,18) . 10. Management of persistent raised ICP in the ICU If despite the above treatment, the patient continues to show evidence of raised ICP, further measures to tackle refractory raised ICP must be instituted. Specific surgically correctible lesions should be attended to. While steroids should not be used for ICP related to infarcts, hemorrhage or trauma, the use of dexamethasone for vasogenic edema related to tumors, granulomas and abscesses can lead to dramatic reduction in lesion volume(10). Head end elevation by 30º (provided patient not hypotensive)(30) and avoidance of neck kinking are important. Fever, agitation and seizures must be assiduously controlled as they can cause massive increases in CBF and CPP(9-12). If ventilated, the PaCO2 should be maintained in the low 30s in order to prevent cerebral ischemia(9-12,31). More extreme hypocapnia can be employed as a short- term temporizing measure for acute deterioration(10,11). Barbiturate coma(9,18,19) and/or mild hypothermia(19,32) are used in some centers in order to reduce the cerebral metabolic rate for oxygen (CMRO2) and thus the cerebral blood flow, although most references pertain to adults(32). Hypotension during barbiturate use may require vasopressors to optimize the MAP/CPP(10,12) . In ICP refractory to medical measures, surgical decompression has been shown to improve survival and functional out-come(33). Acknowledgements Some of the issues covered in the manuscript were discussed during the panel discussion on "Stabilization of a comatose child". This was a sub-specialty "Meet the expert" session of the Intensive chapter of IAP conducted during the 41st Pedicon held at Chennai on 10th Jan 2004 Moderators: Dr. Suchitra Ranjit, Dr Nirmal Choraria. Panelists: Krishan Chugh (Sir Ganga Ram Hospital, Delhi), N Janakiraman (Chicago, USA), Pravin Khilnani (Apollo Indraprastha, Delhi), Indumathy Santhanam (Institute of Child Health and Hospital for Children, Chennai), Sunit Singhi (Post Graduate Institute of Medical Education and Research, Chandi-garh), Soonu Udani (PD Hinduja Hospital, Mumbai). The author also acknowledges with gratitude the expert comments and suggestions of Dr. Venkatakrishna Rajajee, Consultant in Neurocritical Care, Apollo Hospitals, Chennai.
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