Approach to patient with altered sensorium

Approach to a case of Altered Mental Status

1. PATIENT WITH ALTERED SENSORIUM-AN APPROACH MODERATOR & CHAIRPERSON: DR. MANOJ KUMAR (MD ASSOC. PROF.) SPEAKER: DR. SUDHIR KUMAR YADAV (JR-II)

2. Altered m ental status(AMS) or Altered level of consciousness(ALOC) Vague non descript terms patients with seizures, speech difficulties, generalized weakness, anger management issues, hemiparesis, psychosis, etc . Not a disease per se

3. Normal consciousness Arousal Mediated by RAS Situated in brain stem Depressed-lethargy, stupor, coma Elevated- hypervigilant , agitated Cognition Function of cortical hemisphere Confusion, amnesia, hallucination, detachment from reality

4. Level of consciousness Conscious Alert attentive and co-operative Drowsy Patient is sleepy but can be aroused easily by external stimuli. Stupor Appears to be asleep, can be aroused by painful stimuli. Coma Deeply unconscious and non responsive to any stimuli. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale. Lancet 1974; 2:81-4.

5. Common terms related to altered sensorium Confusion A mental and behavioural state of reduced comprehension, coherence and capacity to reason Delirium Acute confusional state defined as relatively acute decline in consciousness that fluctuate over hours or day Hallmark is attention deficit Hyperactive/ hypoactive Dementia Impaired cognitive function in the setting of a normal conscious level. Amnesia A loss of past memories and to an ability to form new ones, despite alert and normal attentiveness Psychosis Refers to a mental state often described as involving a "loss of contact with reality".

6. Differential diagnosis Metabolic/Endo Medication/toxin Infectious Trauma Structural CNS Hypoperfusion state (shock) Delirium Na derangement Ca derangement Glc derangement Thyroid dis HTN encephalopathy HTN meds steroids Sedatives/ analgesics anticonvulsants Alcohols Street drugs Household poisons Polypharmacy Primary CNS Meningitis/encephalitis Brain abscess Secondary effects from any other source of infection: UTI Pneumonia Viral/flu Intra-abdominal Skin/ ulcers Bleeding Diffuse axonal injury Tumor HTN encephalopathy Stroke ( isch or hem) Cardiogenic (MI/CHF) Distributive (septic) Hypovolemic (dehydration) Hemorrhagic ( GIBleed / anemia ) Dementia Unlikely as primary cause- All above may worsen existing dementia Unlikely as primary cause- All above may worsen existing dementia Unlikely as primary cause- All above may worsen existing dementia Unlikely as primary cause- All above may worsen existing dementia Multi infarct dementia Degenerative forms of dementia (Alz, ETOH, post-traumatic) Unlikely as primary cause- All above may worsen existing dementia Psychosis Unlikely as primary cause- All above may worsen existing dementia Noncompliance is common cause of acute psycosis exacerbations. Unlikely as primary cause- All above may worsen existing dementia Unlikely as primary cause- All above may worsen existing dementia Unlikely as primary cause- All above may worsen existing dementia Unlikely as primary cause- All above may worsen existing dementia Unlikely as primary cause- All above may worsen existing dementia

7. Initial Actions and Primary Survey A Airway Open the airway, check pulse- oxymetry and provide supplemental oxygen. Hypoxia can cause AMS. B Breathing Inadequate ventilation will lead to high levels of CO2 and respiratory acidosis. C Circulation Poor circulation leads to hypoperfusion of the brain leads to in adequate oxygen and glucose leading to altered mental status D Gross assessment of disability level. GCS or AVPU for level of consciousness. Note any spontaneous movements: Is there lack of movement on one side of the body (stroke)? Is there lack of movement below a certain level of the body (cord injury)? Is there evidence of seizure activity? Are the pupils equal and reactive? E Exposure and rapid head to toe look for signs of trauma, transdermal drug patches, dialysis devices, infectious sources (such as catheters) or petechiae .

8. What minimum?????? Assessment of the ABC's Cardiac monitoring and pulse oximetry Supplemental oxygen Bedside glucose testing Intravenous access Evaluation for signs of trauma and consider c-spine stabilization Consider naloxone administration if narcotic overdose is suspected

9. Detailed History and Physical Exam Patients with an AS are difficult to derive a comprehensive and detailed history from. Family, friends, caretakers, nursing home workers, witnesses are all invaluable sources of information. Make the effort to contact them to ascertain the nature of the change in mental status. Diabetes (DKA, H O NK), Hypertension (hypertensive encephalopathy or medication overdose) Endocrine disease (thyroid, Addisons ) Renal failure Cancer ( paraneoplastic syndromes, Na+, Ca ++) Cardiovascular and cerebrovascular disease Seizure (atypical?) Psychiatric issues Medication effects are also very common causes of AS in the elderly. A detailed review of medications (including non prescription, health supplements, home remedies) is critical. Has the patient recently started or stopped any medications?

10. Physical examination Vital signs : Is there a fever? Is there adequate blood pressure to perfuse the brain? Is the respiratory rate normal (hypoxia or compensating for acidosis) Neurologic status : Check for level of alertness, GCS of AVPU score.

11. Glasgow Coma Scale

12. Avpu system A lert V erbal responsive to  P ainful stimuli, or U nresponsive

13. Physical examination C ontent of thought and speech?   Does she stay focused? Is her speech tangential? Is she oriented appropriately? Is she concerned about the issue (insight)? Does she keep asking the same questions over? Is she reacting to internal stimuli? Assess for focal motor or sensory findings . Is there weakness or pronator drift? Cranial nerve exam (especially pupils) Watch for tremulousness or abnormal reflexes . DESCRIPTIONS INTERPRETATION Small, reactive Metabolic causes Diencephalic lesion Midposition, fixed Mid brain lesion large, fixed Extensive brain stem lesion hyp oxia S edative overdose A nticholinergic poisoning Pin point Pontine lesion Opiates Unilateral fixed dilated Oculomotor nerve palsy

14. Physical examination Cardiovascular exam : Are there arrhythmias (a-fib) that predispose to embolic strokes? Are there murmurs that indicate cardiac outflow obstruction? Is there evidence of good peripheral circulation? Are there pulmonary findings that indicate pneumonia (sepsis) or pulmonary edema (hypoxia)? Are there bruits over the carotid arteries?

15. Physical examination Abdominal exam : Is there ascites, caput medusa, liver enlargement or tenderness (hepatic encephalopathy)? Is the belly tender (appendicitis, intussusception, abdominal sepsis source, mesenteric ischemia)? Are there scars (renal transplant)?

16. Physical examination Genitourinary and rectal exam : Is the patient making urine? (uremic encephalopathy)? Signs or urinary, vaginal, prostatic or perineal infection? Is there melena or blood in the stool? (hepatic or uremic encephalopathy)?

17. Physical examination Skin, extremity, musculoskeletal exam : Are there petechiae (meningococcemia) Is there a dialysis shunt? (uremic encephalopathy). Are there track marks from injection drug abuse? Are there transdermal drug patches? Is the skin jaundiced (hepatic encephalopathy)? Is there nuchal rigidity or meningismus (CNS infection)? Are there signs of trauma? (raccoon eyes, Battle Ôs sign, hemotympanum )? Are there infectious sources noted (decubitus ulcers, cellulitis, abscesses)? Are there masses or lymphadenopathy that might indicate cancer ( paraneoplastic syndromes)?

18. Categorizing Causes of AMS Finding Delirium dementia psychosis Onset Rapid Slow Variable Course Fluctuating Progressive Variable Vital signs Often abnormal Usually normal Usually normal Level of consciousness Altered Normal Variable Hallucinations Visual (related to external stimuli) Rare Auditory (related to internal stimuli) Physical exam Often abnormal Often normal Often normal Prognosis Poor if cause not tx Progressive Variable Underlying cause Organic (myriad) Organic (degenerative) Functional

19. AS/ COMA LOCALIZING SIGN NO LOCALIZING SIGN SUPRATENTORIAL INFRATENTORIAL NO STIFF NECK STIFF NECK - CVD - TUMOUR - ABSCESS STRU C TURAL DAMAGE FUNCTIONAL NEURONAL DEPRESSION - HYPOXIA - CARDIAC ARREST - ENCEPHALITIS - HEPATIC - URAEMIC - POST ICTAL STATE - FLUID ELECTROLYTE IMBALANCE - DRUGS - SAH - MENINGITIS A Alcohol E Epilepsy, electrolyte, encephalopathy I Insulin O Opiates, oxygen U Uraemia T Trauma Temperature I Infection P Poison, Psychosis S Shock, Stroke, SAH, Space occupying lesion

20. Diagnostic Testing Metabolic or Endocrine Toxic or Medications Infectious Rapid glucose measurement Serum osmolality (HHNK) Serum electrolytes ( esp Na, Ca ) ABG (with co- oxymetry for carboxy - or met- hemoglobinemia ) BUN/ Creatanine Thyroid function tests Serum cortisol level Levels of medications (anticonvulsants, digoxin, theophylline,etc) Drug screen (street drugs, sedatives, narcotics) Alcohol level Serum osmolality (toxic alcohols) CBC with differential Urinalysis and culture (UCG if appropriate) Blood cultures and gram stain Chest X-ray Lumbar puncture (with opening pressure) - Always CT first if you suspect increased ICP, to avoid herniation. Traumatic Neurologic Hemodynamic Instability Head CT/ cervical spine CT X-ray of any areas with trauma or deformity Head CT (without and with if mass lesion or localized infection suspected MRI (if brainstem/posterior fossa pathology suspected) EEG (if non-convulsive status epilepticus suspected) EKG Cardiac enzymes (silent MI) Cardiac echo Carotid/vertebral artery ultrasound

21. treatment As soon as immediate life threats such as impending cardiopulmonary collapse has been intervened treatment should be directed towards correcting / treating the underlying aetiology. "coma cocktail" T = Thiamine O = Oxygen N = Naloxone G = Glucose (Bledsoe BE. No more coma cocktails. Using science to dispel myths & improve patient care . JEMS. 2002 Nov;27(11):54-60.)

22. treatment Trauma emergent head (and often c-spine) NCCT . avoiding any hypoxia or hypotension, to avoid inflicting secondary injury to salvageable brain. Signs of elevated intracranial pressure elevating the head of the bed and avoiding excessive hypertension. Mannitol and hyperventilation. neurosurgery .

23. treatment Infectious causes Fever, recent history of infection or any signs of infection on physical exam need to be addressed immediately. Paracetamol (650-1000mg PO or PR) will help bring down fevers. Headache , neck stiffness, seizures or focal neurologic findings raise CNS infection to the top of the differential then empiric antimicrobials should be started immediately (ex: 2 g ceftriaxone, 1 g vancomycin , ampicillin in listeria risk groups, 800mg ?? acyclovir). If any other sources of infection, appropriate antibiotics (and cultures) should be started right away. Indwelling lines need to be removed or changed and any fluid collections must be drained.

24. treatment Medications, drugs and poisons Overdoses from narcotic analgesics and benzodiazepines can be both diagnoses and treated by use of reversal agents (naloxone and flumazenil, respectively ). An ECG can give clues to overdoses of TCAs (wide QRS ) beta-blockers/CCB/digoxin (bradycardia and variable conduction blocks). All patients with overdose presentation should be screened for suicidality and possible psychiatric intervention.

25. treatment Withdrawal states alcohol and benzodiazepine withdrawal : Rapid fluctuations in mental status May be life-threatening. supportive care, seizure control and often replacing the substance . Narcotic withdrawal not life-threatening . Patients frequently experience formication, nausea, vomiting, diarrhoea and subsequent dehydration. Replacement of narcotics (or partial agonist/antagonists like methadone) will alleviate the symptoms .

26. treatment Metabolic causes Hypoglycemia cannot quickly determine blood glucose go ahead and give an amp of D50 . Refractory hypoglycemia can be treated with glucose drips, glucagon and octreotide . Hyponatremia can cause seizures and these should be treated with benzodiazepines and supportive care. Hypernatremia should respond to appropriate rehydration. Admit these patients into the hospital for further workup of the underlying cause.

27. treatment Metabolic causes Hypo and hypercalcemia : The EKG can give clues. Hype R calcemia causes sho R t QT hyp O calcemia causes l O ng QT. Treatment is supportive admitted for further workup of the causes . Hyper and hypothermia Always obtain a rapid core temperature . Aggressive cooling or rewarming and supportive care are the mainstays of treatment. These patients need admission for workup unless the underlying cause can be recognized, treated and other systemic injury ruled out.

28. treatment Metabolic causes Hypertensive encephalopathy Elevated BP, papillary edema and altered mental status. need ICU level admission Diagnosis (and treatment) is made by lowering the blood pressure and observing the response. lowering the MAP 20-25% will alleviate the symptoms. Lowering blood pressure further can result in cerebral hypo-perfusion and stroke. For this reason the BP is always treated with short-acting rapidly titratable medications ( nitroprusside , esmolol , nicardipine , etc ) and frequent (arterial line) blood pressure measurements. Avoid uncontrollable medications like clonidine in this situation .

29. treatment Primary CNS Causes Seizures Check for hypoglycaemia, treat acute seizures with benzodiazepines, and provide supportive care. Send blood for levels if the patient is on anticonvulsants with measurable levels or metabolites. New onset seizures require a head CT and electrolyte panel at a minimum. Tumors IV contrast enhances the ability of plain CT to identify tumors . If there is evidence of edema and mass-effect on CT, steroids (8-10 mg dexamethasone IV) can help reduce vasogenic edema . Obtain emergent neurosurgical consult and consider admission to an ICU or closely monitored setting for further workup. Focal neurological infections (brain abscess, toxoplasmosis ) These are most prominent in immunocompromised patients. Contrasted head CT should reveal these processes. Begin antimicrobial treatment and consult neurosurgery for admission and management.

30. treatment Primary CNS Causes Strokes almost always have focal findings. obtain a rapid plain head CT (to rule out bleeding ) Ischemic stroke Acute presentations (less that 3 hours) should be considered for fibrinolytic therapy. Haemorrhagic strokes Plain head CT shows acute bleeding well. Like with traumatic bleeds, consult neurosurgery immediately, assess and correct coagulopathic states and provide supportive care. Dementia syndromes history of progrssive worsening of cognitive function coupled with a normal sensorium and normal physical exam is highly suggestive. 

31. Disposition dependent on many factors: How sick is the patient? Is the cause identifiable? Has the cause been fixed? Did the patient return to normal? Is the situation likely to return? If it does return, is there adequate social support to recognize it and bring the patient in for medical care? Patients who have an identifiable and treatable aetiology ( hypoglycemia from a diabetic missing a meal, a seizure patient out of phenytoin) can usually be discharged with appropriate follow-up. Any time the aetiology cannot be ascertained clearly, the patient should probably be admitted for observation and further work-up.

32. Thank you Take home msg. Altered sensorium is not a disease per-se. Causes may span from benign rapidly reversible to life threatening. Organic causes must be rule out before labelling psychosis. Rapid primary survey is done to secure ABCs the detailed history & examination is done followed by indicated investigations keeping in mind the reversible and life threating causes especially. In trauma is suspected NCCT head is obtained, if CNS infection is suspected empirical antibiotic given, hypoglycaemia should be reversed with 50D or 25D, other aetiologies should be managed acc. to recent guidelines.