Approach to a child with altered sensorium DD

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A systematic approach


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Dinesh Dharel MD Paediatrics Resident IOM:

Dinesh Dharel MD Paediatrics Resident IOM Approach to a Child With Altered Sensorium


Contents: States of altered consciousness Glasgow Coma Scale Pathophysiology Causes Approach Emergency management History Examination Investigations Treatment Algorithm for approach to diagnosis

What is consciousness?:

What is consciousness? “state of wakefulness and awareness of self and surroundings” (Abend et al., Rogers’ Handbook of Pediatric Intensive Care Medicine, 2009, p. 256) A conscious individual is: Aware of himself and environment, Capable of responding correctly to verbal and mechanical stimuli and Able to recall past events. Two neurophysiologic functions: Arousal Awareness

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Alert: Fully conscious Lethargic: appear somnolent, but may be able to maintain arousal Obtunded: requires touch or voice to maintain arousal Stuporous: unresponsiveness from which the individual can be aroused only by painful stimulus Comatose: State in which the patient is unable to arouse or respond to noxious stimuli and is completely unaware of self and surroundings Levels of Consciousness:

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A The child is awake, alert, and interactive with parents and care providers V The child responds only if the care provider or parents call the child's name or speak loudly P The child responds only to painful stimuli, such as pinching the nail bed of a toe or finger U The child is unresponsive to all stimuli From Ralston M, Hazinski MF, Zaritsky AL, et al, editors: PALS course guide and PALS provider manual: Dallas, 2007, American Heart Association. AVPU NEUROLOGIC ASSESSMENT

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GCS: BEST EYE OPENING Spontaneous 4 To voice 3 To pain 2 None 1 GCS: BEST MOTOR RESPONSE Obeys 6 Localizes pain 5 Withdraws 4 Flexion 3 Extension 2 None 1 In infants And small children Spontaneous and purposeful movement = 6 Withdrawal in response to touch = 5

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GCS: BEST VERBAL RESPONSE OLDER CHILDREN INFANTS AND YOUNG CHILDREN Oriented 5 Appropriate words; smiles, fixes, and follows 5 Confused 4 Consolable crying 4 Inappropriate 3 Persistently irritable 3 Incomprehensible 2 Restless, agitated 2 None 1 None 1 Adapted and modified from Teasdale G, Jennett B: Assessment of coma and impaired consciousness: a practical scale, Lancet 2:81–84, 1974. Published in Nelson Textbook of Pediatrics, 9 th edition

Significance of GCS::

Significance of GCS: Mainly in Head Injury: Mild – 13-15, Moderate – 9-12, Severe – 3-8 Fall of GCS of 2 or more – Indicates deterioration and need of active intervention Coma is defined as: No eye opening (1), No recognizable words uttered (2 ), Not obeying commands (5), ie, score = 8 or less. GCS score ≤8 require aggressive management, including endotracheal intubation and mechanical ventilation and placement of an ICP monitoring device. Prediction of prognosis of comatose child: GCS >8: Good chances of recovery GCS 3-5: Fatal brain damage

Clinical assessment of acute coma in children: Gemke a , Tasker The Lancet, Volume 351, Issue 9107, Pages 926 - 927, 28 March 1998:

Clinical assessment of acute coma in children: Gemke a , Tasker The Lancet, Volume 351, Issue 9107 , Pages 926 - 927, 28 March 1998 Persistent CNS damage remains a major cause of mortality and long-term morbidity in children who sustain acute traumatic or non-traumatic brain injury. In children coma is the most prominent clinical presentation of acute brain injury which, if by trauma, may set in after a longer lucid interval than in adults. The Glasgow coma scale (GCS) devised for the clinical assessment of the progression of the central syndrome, is used primarily for bedside monitoring of the degree of impairment of consciousness. In the initial phase of the injury, such cortically determined functions are very helpful as reliable measures of change when used by experienced and highly trained observers.

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The GCS requires an adult level of development. So, modifications of the GCS have been introduced and found to be valid for assessing children whose neurodevelopmental function is below 10 years. An assessment of the merits of six different coma scales in paediatric practice showed that interobserver agreement was highest for the paediatric coma scale,which includes age-adjusted verbal and motor-response scores. A recent study in intubated children has suggested that a grimace score, as a surrogate of cortical assessment, might overcome the difficulty of assessing verbal response in these patients. In post-traumatic head injury in adults, a GCS of 8 or less signifies a high likelihood of raised intracranial pressure and the need for a strict regimen of special care.


Pathophysiology: Consciousness depends on proper function of cerebral cortex and the ARAS Stimulation: alert conscious state Suppression: sleep or drowsiness Increased neuronal excitability  Restless/Confusion Tremor/Delirium Stupor Coma Decreased neuronal excitability Lethargic  Obtunded Stupor Coma

Grades of Coma:

Grades of Coma Stage 1 : Stupor Stage 2: Light coma Stage 3: Deep coma Stage 4: Brain Death

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Diminished alertness may be due to: Damage to RAS or its projections Destruction of B/L cerebral hemispheres Suppression of reticulocerebral function by drugs/toxins or by metabolic derangements like hypoglycemia, acidosis Pathophysiology:

Reticular Activating system::

Reticular Activating system:

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Monroe-Kellie doctrine Cranium-rigid structure with fixed volume (not completely true if open fontanel present) For ICP to remain constant, an increase in one component, must be accompanied by a decrease in another. Mechanisms of Increased ICP Brain  Cerebral edema Blood  Increased CBF CSF  Hydrocephalus Space Occupying Lesion Tumor/Hematoma brain 80% blood 10% CSF 10% Pathophysiology:

Causes of Altered Sensorium::

Causes of Altered Sensorium: Infectious disorders: Bacterial – Meningitis Viral – Meningitis, Encephalitis, Postinfectious encephalomyelitis Cerebral Malaria Lyme disease, Rocky Mountain Spotted Fever Brain abscess, Subdural empyema Sepsis Poisoning, Narcotics, toxins, Drugs: Ethanol Anticonvulsant wild mushroom


Causes: Metabolic disturbances Hypoglycemia, Diabetic ketoacidosis Dyselectrolytemia: Hyponatremia, Hypernatremia, Hypocalcemia Renal causes: Uremic encephalopathy Hepatic encephalopathy Inborn Errors of Metabolism – Glycogen storage disorders, Medium chain acyl-CoA dehydrogenase deficiency Endocrine causes: Adrenal insufficiency Hypoparathyroidism Thyroid disorders


Causes: Head Injury: Concussion, Contusion, Diffuse Axonal Injury Intracranial hemorrhage (Epidural, Subdural, Subarachnoid, Intracerebral hemorrhage) Epilepsy: Post-ictal, Status epilepticus Increased ICP: Intracranial SOL: Brain tumours, Brain abscess Hydrocephalus, Cerebral oedema, ICH Reyes syndrome


Causes: Vascular: Intracerebral/ Subarachnoid hemorrhage Cerebral vein thrombosis, vascular malformation Emboli – Bacterial endocarditis SLE Hypertensive Encephalopathy Hypoxia-Ischemia Hypotension, Cardiac arrest/arrhythmia, Near-drowning Psychological

Approach to a child with altered sensorium:

Approach to a child with altered sensorium General assessment: Appearance Work of breathing Colour of skin Primary assessment: Airway Breathing Circulation Disability (GCS) Exposure Signifies emergency situation and requires urgent assessment May require immediate intervention for life threatening condition at any point in the assessment

Approach: stabilization:

Approach: stabilization ABCs of Resuscitation Open airway, may require advanced airway Oxygen at high flow, may require positive pressure ventilation Consider intubation if apnea, hypoventilation or unable to protect airway Check RBS. Correct hypoglycemia. Correct fluid and electrolyte imbalance, may require vasopressors. Stabilise the cervical spine in trauma cases Check for features of raised ICP

Approach: Decision point:

Approach: Decision point Increased ICP  Must act immediately ( Elevate the HOB 30 degrees, Hyperventilate, Mannitol 1 g/kg or 3% NaCl, Urgent CT head, Neurosurgical consultation) No increased ICP  Time to consider workup


approach—History : Rapid initial history: SAMPLE Signs and Symptoms at presentation Allergy Medication, drugs or toxins Past medical history and significant family history Last meal Events prior to mental status changes Follow-up with more complete history:

approach—focused Physical Exam:

approach—focused Physical Exam Rapid neurological examination: Pattern of respiration Size and reactivity of pupil Eye movements (spontaneous or induced) Motor responses Systemic Exam: Vital Signs, Signs of trauma, Signs of infection, Signs of bleeding, Signs of other systemic illnesses Best motor response Score Obeys 6 Localizes 5 Withdraws 4 Abnormal flexion 3 Extensor Response 2 None 1

Approach: History:

Approach: History Unconscious child – No witness or Hx s/o ↑ or ↓ neuronal excitability Age: Onset: Acute/Sudden – CVA, Head Trauma, toxins, postictal, acute hypoxia Insidious– Brain tumours Infant Child Adolescent CNS infection Ingestion Drug/Alcohol overdose Inborn errors of metabolism CNS infection Intentional poisoning Metabolic disorders Seizure Trauma Abuse / Trauma Abuse / Trauma

Approach: History:

Approach: History Associated symptoms of CNS causes: Fever – Infections Headache, Vomiting, Diplopia, personality changes – Increased ICP Neck stiffness – Meningitis, SAH Rash - Meningococcemia H/o excess cry, irritability, enlarging head in infants – Meningitis, Hydrocephalus H/o Trauma (Severity, Bleeding from ear/nose) Seizures – ICH, ICSOL, Epilepsy, Post-ictal Recurrent episodes: Epilepsy, Hypoglycemia, Substance abuse, Inborn errors of metabolism H/o recent infectious diseases – eg. Mumps (Parotid swelling), measles (rash)

History: Presence or absence of fnd:

History: Presence or absence of fnd NO FND: CSF Normal NO FND: CSF Abnormal Poisons, toxins, narcotic agents Meningitis Metabolic d/o: hypoglycemia, uremia, DKA, hepatic encephalopathy Encephalitis Head injury SAH Septicemia Cerebral vein thrombosis Post- ictal Midline cerebral tumors Hyperpyrexia Hydrocephalus Water intoxication Lead poisoning FND: CSF Normal FND: CSF Abnormal Demyelinating disorders Brain abscess, Subdural empyema Post- ictal coma HSV Encephalitis Intracerebral hemorrage Head injury, Intracranial hemorrhage Tumors Vascular malformations FND: Paucity of movement of limbs, Diplopia, Squint, Facial deviation, Nasal regurgitation, Difficulty swallowing

Approach: History:

Approach: History Failure to thrive, vomiting, peculiar skin odour – Metabolic cause Jaundice, abdominal distension, hematemesis , melena , bleeding - Hepatic encephalopathy ↓ Urine output, swelling, periorbital puffiness, Nausea, vomiting, loss of appetite – Uremic encephalopathy H/o loose stools- HUS, Hypovolemia Ingestion of toxins/poisons , medications H/o exposure to infections ( Meningococcus ) H/o Immunocompromised state ( Cryptococcal meningitis, TBM), malignancy H/o visit to endemic regions (Malaria, JE) Family h/o TB, migraine, epilepsy Birth H/o: Birth asphyxia, h/o recurrent hypoglycemia Developmental delay or regression

Not to miss points:

Not to miss points Is there associated fever? May indicate a self-limited infection, encephalitis, meningitis, cerebral abscess or cerebral hemorrhage. Is there a history of trauma? Suspect a subdural or epidural hematoma and concussion. Is there a history of drug (cocaine, LSD, phencyclidine) or alcohol ingestion? Are there focal neurologic signs? Think of subdural or epidural hematoma, cerebral abscess, or cerebral hemorrhage, thrombosis or embolism Is there nuchal rigidity? meningitis or SAH Is there a sweet odor to the breath? Diabetic coma or alcoholism. What is the response to intravenous thiamine? Wernicke's encephalopathy or Korsakoff's syndrome. Intermittent delirium? psychomotor epilepsy and transient global amnesia.

Approach: Examination:

Approach: Examination Vital signs: HR: Bradycardia (↑ ICP), Tachycardia (Shock, Infections, Atropine); Irregular (Arrhythmia) BP: (HTN in ↑ICP, HTN encephalopathy, cocaine), Hypotension (shock, barbiturates) Temp: Fever in Infections, Hyperpyrexia, Hypothalamic lesion or pontine hemorrhage, atropine poisoning, Hypothermia in Sepsis, shock, alcohol, barbiturate poisoning, hypoglycemia RR : Bradypnea/ Apnea (Drug intoxication, septicemia), Tachypnea (Metabolic Acidosis, Brainstem lesions, Pneumonia), Cheyne-Stoke breathing (B/L cortical damage with intact brainstem), Irregular (medulla involved)

Respiratory patterns::

Respiratory patterns: Cheyne-Stokes Central Hyperventilation Apneustic Cluster breathing/Gasping Agonal breathing Hemispheric Midbrain Mid/Lower Pons Low Pons/Upper Medulla Medulla Location Pattern of b reathing

Pupils: Size and Reactivity:

Pupils: Size and Reactivity Midbrain damage – Moderately dilated, slight fluctuation Pontine lesions- Pinpoint pupils Severe Ischemic Brain Damage – B/L fixed, dilated III CN compression (impending uncal herniation) - U/L fixed dilated Hypothalamic or lateral medullary lesions: U/L constricted Metabolic, toxic causes of coma - Equal and reactive except atropine, Belladona poisoning or TCA overdose (dilated unreactive); opiate, clonidine, cocaine, amphetamine overdose or organophosphate poisoning (pinpoint)

Eye Movements::

Eye Movements: Oculocephalic or Doll’s eye response: Shows Intact Brainstem. Oculovestibular response: Lost in pontine lesions, labyrinthitis, Sedatives, Phenytoin induced coma Both lost but intact pupillary reflexes present in metabolic encephalopathy Stimulation of cortical centre for gaze e.g. seizure focus → conjugate deviation of eye to contralateral side Destructive lesion at gaze centre → conjugate deviation of eye to same side Hypertropia: Brainstem/Cerebellar lesions

Motor Examination::

Motor Examination: C/L Monoplegia , Hemiplegia with hemifacial weakness with Change in tone or DTR – C/L Cortical or subcortical lesions Plantars - B/L upgoing in deep coma, U/L upgoing in C/L UMN lesions Involuntary movements: Repetitive, multifocal, myoclonic jerks in anoxic, metabolic or toxic encephalopathies Seizures FND – Postictal coma, Tumours, Brain abscess, Subdural Empyema , Encephalitis, Head injury , Intracranial hemorrhage, Vascular malformation Flaccidity: Loss of all cortical & brainstem function

Abnormal posture:

Abnormal posture Progressive compression of descending motor tracts Decorticate posturing: flexion at wrist and elbow extension of legs and feet  lesion above midbrain Decerebrate posturing: external rotation of upper extremity, flexion at wrist internal rotation of legs, extension of legs and feet  lesion below midbrain  raised ICP

Cranial Nerve Exam::

Cranial Nerve Exam : Use to assess various level of function Midbrain—III (Pupillary changes) Pons—V, VII (Corneal reflex) Upper Medulla—IX, X ( Gag and Cough reflexes) Lower Medulla—XI III, IV, VI  Eye movements (Doll’s eyes) VIII  Occulovestibular reflex (Calorics)

Fundoscopic exam::

Fundoscopic exam: Disc changes with papilledema Normal Early papilledema Moderate papilledema with early hemorrhage Severe papilledema with extensive hemorrhage Subhyaloid hemorrhages in subarachnoid hemorrhage Hypertensive retinopathy: exudates, hemorrhages, papilloedema Choroid tubercles - TBM

Approach: Other CNS examination:

Approach: Other CNS examination Anterior fontanelle Signs of meningeal irritation Signs of raised ICP Speech Sensory, Coordination – difficult to assess No FND or meningial signs- Drugs, metabolic d/o or seizure Metabolic coma- symmetrical hemispheric responses (eg Asterixis) with intact brainstem function

Approach: examination:

Approach: examination Any signs of trauma (Scalp laceration/swelling/fracture, ENT Bleeding) Pallor - hypoxia, bleeding disorders Icterus – Hepatic encephalopathy, Sepsis Cyanosis – Cyanotic congenital heart disease, Hypoxia Oedema – CHF, Renal failure Dehydration – Hypovolemic shock, HUS Skin- Meningococcal rash, Petechiae CVS: Arrhythmias, Murmurs (Congenital heart disease, Infective endocarditis) Chest: Signs of chronic lung disease P/A: Tender hepatomegaly (Hepatitis, Sepsis), Hepatosplenomegaly- malaria

Approach: Investigations::

Approach: Investigations: Random Blood Sugar- Urgent Ammonia, lactate, ABG Serum Na, K , Urea, Creatinine , Ca, Mg, Phosphorus, uric acid, amino acids CBC , Clotting screen, ESR, CRP Blood C/S, JE Serology, PCR LFT , TFT, autoimmune screen CXR Urine ketone, WBC, RBC , C/S Urine amino acids, organic acids, orotic acid Gastric aspirate, Blood or urine for toxicology

Approach: Investigations::

Approach: Investigations: CT Scan Head Urgent if SAH suspected Before LP if Raised ICP, FND or Comatose If impending herniation , intubate , hyperventilate and control ICP before CT scan CECT or MRI of head Intracranial SOL –tumours, abscess, hematoma, NCC, Tuberculoma Hydrocephalus, infarction, structural anomalies EEG Lumbar puncture CSF for TC, DC, Protein, Sugar, Gram stain, C/S, PCR, Glycine Relative Containdications of LP to be considered

Approach: Treatment::

Approach: Treatment: Initial stabilization, consider ICU care Correct fluid and electrolyte imbalance Catheterisation to monitor I/O, NG tube Bladder/Bowel care, Care of eyes and back T/t Raised ICP (Manitol, 3% saline, Dexamethasone) Manage for Fever or hypothermia Antibiotics, ATT, Antimalarial Hepatic encephalopathy – Lactulose, systemic antibiotics, vitamins, protein restriction Medical management and Dialysis for ARF, CRF Antihypertensives – HTN encephalopathy Corticosteroids – encephalopathies Poisoning – Gastric lavage, Antidotes (Naloxone, Flumazenil, physostigmine)

General Care at home: :

General Care at home: Observe your child carefully for any changes in behavior. Stay with your child if you notice any altered behavior. If your child has diabetes, make sure that any approved medication is given on time and as prescribed. Give your child frequent healthy snacks and meals. Ensure your child is supervised while playing sports. Follow up as advised by the doctor or if any of the following occurs: Fever greater than 100.4°F , Extreme tiredness or difficulty waking; hyperactivity, Lack of interest in the surroundings, Poor muscle tone or limpness, Weak, feeble cry, No eye contact or response to touch or voices, Increased headache or Seizure

Approach to a child with altered sensorium::

Approach to a child with altered sensorium: S/S S/O a progressive intracranial process CT scan Blood glucose level YES NO Abnormal Normal Intracranial haemorrhage Tumors, AV malformation Ruptured aneurysm, Cerebral Edema Brain abscess, Embolism, Stroke Abnormal Normal Hypoglycemia

Approach to a coma patient….:

Approach to a coma patient…. Normal Glucose C/F CNS infection YES NO LP if stable Meningitis encephalitis Detail H/o & physical exam Toxicology screen Additional investigation Normal Abnormal Drug, toxin ingestion Sepsis, metabolic Hypoxic ischemic encephalopathy, Epilepsy, Hemorrhagic shock Reye syndrome CT head Normal Psychiatric, seizure Abnormal Anatomic lesion, AV malformation Embolism, IC Hge, Vasculitis, HTN encephalopathy


Reference: Nelson Textbook Of Pediatrics, 18 th Ed Ghai Essential Pediatrics, 7 th Ed Clinical Pediatric Neurology - Gerald M. Fenichel, 2 nd Ed Harrison’s Textbook of Medicine

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