Evaluation of Altered Mental Status

1. Evaluation of Altered Mental Status Kalpesh Patel, MD Dept. of Pediatric Emergency Medicine October 25, 2006

2. Objectives • To understand the different terms used for level of consciousness. • To understand to pathophysiology behind altered level of consciousness (ALOC). • To review the differential diagnosis for ALOC. • To learn important physical exam findings to clue you into the etiology of ALOC. • To review the basic management of ALOC.

3. Definitions • Consciousness defined as being awake and aware of both one’s self and one’s surroundings. • Age specific responses • Altered Consciousness covers a spectrum of states: • Consciousness • Coma • Lethargy • Confusion/Disorientation • Stupor or Obtunded

4. Definitions • Consciousness • Confusion/Disorientation – occurs in the order of time, place, person, then unconsciousness • Stupor or Obtunded – not totally asleep, but diminished response to external stimuli • Lethargy – Depressed consciousness like a deep sleep state where pt roused, but immediately returns to deep sleep • Coma – complete unawareness and unresponsiveness • States change over time, so pt specific responses are preferable descriptors

5. Epidemiology • Bimodal distribution • Infection accounts for 1/3 of nontraumatic cases • Congenital malformations present in the first few postnatal months • DKA more common in adolescence • Inborn errors present in infancy • Toxic ingestion common in childhood and adolescence • Rate of trauma increases throughout childhood

6. Pathogenesis • Cerebral hemispheres – cognition, affect, perception of themselves and environment • Wakefulness – Ascending Reticular Activating System (ARAS) • Midbrain/pons

7. Pathogenesis • Near cranial nerves II, III, VI, and VIII and MLF • Controls pupillary light reflexes and eye movements • Impingement of cranial nerves suggests impingement of ARAS • Pupillary responses proved the most direct window to the brain

8. Pathophysiolgy • Compression of the ARAS usually results from structural causes • Diffuse cerebral dysfunction usually has a medical basis

9. Etiologies • Altered Level of Consciousness (ALOC): • One of the most difficult diagnostic and management problems in pediatric emergency medicine • Requires quick action to avoid irreversible damage • Wide array of possible diagnoses • ALOC is a symptom of another problem, not a diagnosis itself • Helpful mnemonic is AEIOU TIPS

10. Etiologies • A – Alcohol, Abuse (physical or substance) • E – Encephalopathy, Electrolytes • I – Insulin, Intussusception, Inborn errors • O – Overdose, Oxygen deficiency • U - Uremia • T – Trauma, Temperature abnormality, Tumor • I - Infection • P – Poisoning, Psychiatric, Psychogenic • S – Shock, Stroke, Seizures, Shunt

11. Herniation Syndromes • Increased ICP • Found in many etiologies causing space occupying lesions • Requires immediate identification and action • Focal neurologic signs suggest a structural lesion, lack of focality suggests a medical cause • Exceptions: • Acute hydrocephalus • Bilateral subdural hematomas • Acute bilateral cerebrovascular disease • Encephalopathies with focal signs • Postictal states such as Todd paralysis • Beware of Cushing’s triad – hypertension, bradycardia, irregular respirations

12. Herniation Syndromes • Central herniation • Pressure in both hemispheres • Pushes midbrain and upper brainstem through tentorium • Foramen Magnum (Tonsillar) herniation • Posterior fossa pressure • Pushes cerebellar tonsils through foramen magnum

13. Herniation Syndromes • Cingulate gyrus herniation • Unilateral cerebral hemisphere pressure • Pushes gyrus beneath falx cerebri • Uncal herniation • Unilateral volume increase • Pushes lower midline cerebrum and hippocampal gyrus through tentorium

14. ALOC Clinical Features • 4 pathophysiologic variables are helpful • Respiratory pattern • Pupillary light reflexes • Spontaneous eye movements • Motor responses

15. Respiratory Pattern • Ventilation is governed by lower pons and medulla • Modulated by forebrain cortical centers • Patterns from rostrocaudal involvement • Post-ventilation apnea • lasts 10-30 sec followed by voluntary deep breathing • Forebrain involvement • Cheyne Stokes respirations • Hyperpnea alternating with apnea • Depth of breathing crescendo-decrescendo • Diencephalon of deep cerebral hemispheres • Caused by failing respiratory center of brain

16. Respiratory Pattern • Central neurogenic hyperventilation • Regular and rapid respirations • Normal PaO2 and low PaCO2 • Midbrain • Brain’s attempt to reduce ICP • Apneustic breathing • Deep, gasping inspiration with a pause at full inspiration followed by a brief, insufficient release • Signifies damage to Pons/medulla

17. Pupillary Reflex • Pupillary pathways near ARAS • Pupillary pathways resistant to metabolic insult • Single most important physical finding to distinguish structural vs metabolic disease

18. Pupillary Reflex • Unequal, sluggish or unreactive pupils (1) • Eye is affected is on the side of the lesion (2) • Bilateral enlarged and unreactive pupils indicate massive CNS dysfunction (3) • Drugs also affect pupils • Opiates – pinpoint pupils • Anticholinergics – large pupils

19. Eye Movements • In light stage of coma, roving side-to-side movements occur • Persistent deviation to one side may indicate focal seizure activity • Structural brainstem lesions abolish conjugate eye movements • Oculocephalic reflex (“doll’s eyes”) – hold eyelids open and rotate head from side to side • Normal or positive – conjugate deviation of eyes away from direction of head movement • Contraindicated in c-spine injury • http://prohealthsys.com/physical/movies/cranialnerve_n_13.mov

20. Eye Movements • Oculovestibular reflex – elevate head of bed 30 degrees and inject 10-50ml of ice water into ear canal • Normal response is nystagmus with slow phase towards irrigated ear and fast beats away • Unconscious pt with intact brainstem eyes move towards stimulus and remain tonically deviated for a minute and slowly return to midline • Contraindicated if tympanic membrane not intact

21. Eye Movements • Cerebral lesions – eyes deviated towards side of lesion • Brainstem lesions – eyes deviated away from side of lesion • Setting sun sign – downward deviation of eyes • Upper midbrain lesions and hydrocephalus • Third nerve paralysis – eyes point down and out • http://cim.ucdavis.edu/EyeRelease/Interface/TopFrame.htm • Brief fundoscopic exam should also be performed looking for papilledema or retinal hemorrhages.

22. Motor Responses • Assess muscle strength, tone and deep tendon reflexes for normality and symmetry • Assess if pt can localize motor responses to determine level of brain lesion • Decerebrate posturing – flexion of upper extremities with extension of lower extremities • Lesion in cortex or subcortical white matter

23. Motor Responses • Decorticate posturing – rigid extension of arms and legs • Lesion at brainstem, usually pons • Flaccid – gravest prognosis with lesion deep in brainstem

24. Management • ABC’s with neck immobilization if history of trauma • Bedside glucose • Hyperventilation to PaCO2 of around 35 mm Hg if increased ICP suspected • Increase ventilation until pupils constrict • Support perfusion • Neuro exam • GCS or AVPU • Pupillary response • Respiratory pattern • Treat hypoglycemia with glucose or glucagon IM • Consider Naloxone

25. Management • Formulate presumptive diagnosis using AEIOU TIPS • Pursue specific management • Admit to PICU: • Any pt not responding to therapeutic intervention • Require ongoing monitoring • Diagnosis in question after initial management

26. Prognosis • In general, pediatric coma patients fare better than adults • Predictors of poor outcome • Long (>25 min) duration of cardiac arrest • Blood glucose >250 • Unresponsiveness on arrival • GCS <8 on arrival • pH < 7.10 on presentation • Coma > 24 hours

27. Trauma • Epidural Hematoma • Lens shaped • Caused by arterial rupture • Skull fracture present in 85% of cases

28. Trauma • Subdural hematoma • Crescent shaped • Caused by tearing of bridging veins through dura and arachnoid • Skull fracture present in 30% of cases • Retinal Hemorrhage in 75% of cases

29. Trauma • Cerebral Contusion • Can lead to increased ICP

30. Trauma • Cerebral Edema • Loss of gray-white matter interface • Loss of sulci • Occurs 12-24 hours after injury

31. Seizure • All seizures except petit mal are followed by a post-ictal state • Measure drug levels for children on anticonvulsants • Comatose patients may have non-convulsive seizures needing an EEG to diagnose • Assume intracranial lesion with non-immediate post traumatic seizure or new focal seizure until proven otherwise • Fever- consider meningitis, encephalitis, brain abscess, or febrile seizure

32. Meningitis • Bacterial • Most common infection severe enough to cause profound ALOC • Non-bacterial • Slower onset of symptoms

33. Infection • Brain Abscess • Chronic sinusitis, chronic otitis, dental infection, endocarditis or uncorrected cyanotic congenital heart disease can increase risk

34. Encephalitis • Encephalitis – inflammation of the brain parenchyma usually due to viral infection • Mumps and Measles common before immunization • Varicella – occurs 2-9 days after rash develops • Arthropod – varies by geographic areas and seasonal • HSV – most common devastating cause • Death or permanent neurologic damage in 70% of cases • Affects temporal lobes causing seizures, parenchymal swelling and uncal herniation

35. Tumor • Tumors • Can cause seizure, hemorrhage, increased ICP and can invade into ARAS • Ataxia and vomiting, think infratentorial • Seizure, hemiparesis, speech or intellectual problems, think supratentorial • Headache, lethargy, vomiting, think acute hydrocephalus

36. Stroke (Cerebrovascular) • Hemorrhagic is usually due to aneurysm • Severe headache • “Sentinal bleeds” are common before rupture • Subarachnoid blood is seen • AVM or cavernous hemangioma • Low flow and less acute symptoms

37. Stroke (Cerebrovascular) • Thrombosis or Embolic Stroke • Occlusion of anterior, middle or posterior cerebral artery will NOT cause coma • Carotid infarct can cause coma • Infarcts eventually lead to increased ICP • Cerebellar infarcts rarely have coma • Basilar Artery infarcts cause rapid coma due to brainstem damage

38. Shunts • Placed for hydrocephalus • Malfunction due to mechanical causes or infection • Highest risk of failure in first 6 months after surgery • Intrathecal baclofen pump overdose can cause coma

39. Hypoxia • Neurons extremely sensitive to hypoxia and cease function within seconds of hypoxia • Permanent CNS dysfunction can occur within 4-5 minutes of total anoxia at body temperature • Hypercarbia can also cause neurologic depression and coma

40. Temperature • Hypothermia • Each drop by 1 degree celcius causes a 6% drop in cerebral blood flow • 29-31 degrees – delerium, confusion, muscle rigidity • 25-29 degrees – comatose, no DTR’s, fixed and dialated pupils • Hyperthermia • Headache, vomiting, seizure, obtundation, or coma result especially above 41 degrees C • Infants left in a car exposed to sunlight

41. Hypertension • May lead to cerebral hemorrhage • Hypertensive encephalopathy • Usually due to renal, endocrine or cardiac pathology or toxic ingestion (cocaine) • Headache, N/V, vision changes, ALOC and coma can result • Condition improves once BP has normalized

42. Electrolytes • ALOC may be caused by: • Abnormality in any cation (Na, Ca, Mg, Phosphorus) • Metabolic acidosis or alkalosis • Hyperammonemia from inborn errors, urea cycle • Hypoglycemia – most common cause in pediatrics • Infants and small children have decreased gluconeogensis • SBI, Sepsis, dehydration, ethanol or oral hypoglycemic ingestion are causes • Hyperglycemia – especially new onset diabetes have ALOC due to hyperosmolarity • DKA can lead to cerebral edema

43. Psych • Psychiatric disorders can produce stupor like state • Psychogenic • Neuro exam reveals this • Pt avoids hand falling into face • Resists eyelid opening • Increased heart rate to painful stimulus • Intact neuro exam

44. Other Causes • Renal or Hepatic failure • Hemolytic Uremic Syndrome can cause coma from uremia or from basal ganglia infarction • Reye’s Syndrome • Antecedent viral illness • Mitochondrial injury affects all organs • Severe vomiting followed by combative delirium, then coma • Cerebral edema results leading to central herniation

45. Bibliography • Avner, JR. Altered states of consciousness. Pediatrics in Review 2006;9:331-338 • Gausche-Hill, M, Fuchs, S, Yamamoto, L. APLS The Pediatric Emergency Medicine Resource Revised Fourth Edition. American Academy of Pediatrics and American College of Emergency Physicians, 2007. p147-153. • Fleisher, GR, Ludwig, S, Henretig, FM. Textbook of Pediatric Emergency Medicine Fifth Edition. Lippincott Williams & Wilkins 2006. p201-212. • Kanich W, Brady WJ, et al. Altered mental status: evaluation and etiology in the ED. Am J Emerg Med 2002;20:613-617. • Meyer PG, Ducrocq S, Carli P. Pediatric neurologic emergencies. Curr Opin Crit Care. 2001;36:651-659.