ALTERED MENTAL STATUS & COMA. Medical students

AdanwaliHassan 155 views 37 slides Oct 20, 2024
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About This Presentation

Medical students
Medical students
Medical students


Slide Content

ALTERED MENTAL STATUS & COMA Dr. Adenwali Hassan Ahmed: ( Mwn , Bsc -Medical Doctor, Bsc - Public Health Officer, Msc-Gyn / Obest .

OBJECTIVES 1. To understand the causes of Altered Mental Status (AMS) 2. To develop an approach to the AMS patient 3. To make an appropriate disposition in an altered patient.

INTRODUCTION Altered mental status is a non-specific term referring to patients who have impaired responsiveness or are unresponsive to external stimulation and are either difficult to rouse or are unrouseable Coma is a sleep-like state or “ unrouseable unresponsiveness” Lethargy, stupor (feeling of distress) and obtundation refer to the states between alertness and coma Lethargy & obtundation are similar- A state of comatose torpor (as found in sleeping sickness)

Cont--- Altered mental status is an acute, life-threatening emergency; it requires rapid intervention to preserve brain function and life

CAUSES OF ALTERED MENTAL STATUS AND COMA A decrease in level of consciousness is caused by either: Diffuse CNS dysfunction (toxic-metabolic causes) majority of cases; these conditions impair oxygen or substrate delivery to the brain which alters cerebral metabolism or interferes with neuronal function; or

Cont--- Primary CNS disease or trauma – either: Injury to bilateral cerebral hemispheres (diffuse trauma, ischemia); or Structural injury to the reticular activation system (RAS) in the brainstem; caused by: Direct “hit” (hemorrhage, brainstem stroke) Indirectly from compression ( tumour , subdural or epidural hematoma).

Cont--- Pneumonic for possible causes of coma is “TIPS” AND “AEIOU”: Trauma/Temperature Infection (CNS or other) Poisoning/Psychiatric Space-occupying lesions/Stroke

Cont--- AEIOU Alcohol/Acidosis Epilepsy ( nonconvulsive status epilepticus , post- ictal state)/Endocrine Insulin (hypoglycemia, hyperglycemia) Oxygen (hypoxia) Uremia

EMERGENCY EVALUATION AND MANAGEMENT OF AMS AND COMA 1. Initial Approach – ABCD: 1. Airway: if patient is deeply comatose, endotracheal intubation needs to be considered. indications for intubation include in the Altered LOC patient include: Airway protection in reduced LOC, GCS 8 or less The need to provide positive pressure ventilation, poor oxygen saturation despite supplemental oxygen Predicted deterioration, i.e. in cases of shock or head injury with signs of increased intracranial pressure.

Cont--- 2. Breathing: • supplemental oxygen should be given on all patients with AMS.

Cont--- 3. Circulation/C-spine: Adequate cerebral perfusion is critical in AMS patients; maintain systemic blood pressure at a mean arterial pressure (MAP) of at least 80 mm Hg Ensure adequate IV access to facilitate above Ensure C-spine stabilization in potential trauma patient

Cont--- 4. Drugs: Administer appropriate universal antidotes (“DON’T”): Dextrose: one ampule D50W if low blood sugar Naloxone : 0.4 – 2mg IV or IM if opiate use is suspected, (often lower initial doses are used) Thiamine: 100mg IV if history of alcohol abuse or malnourished Note: Flumazenil (a benzodiazepine antagonist) is not indicated in the treatment of an undiagnosed coma patient.

2. Vital Signs: Extreme hypertension may suggest hypertensive encephalopathy or hypertensive intracerebral / cerebellar /brainstem hemorrhage Hypotension may reflect sepsis, hypovolemia , cardiac failure or drug ingestion Hyperthermia usually signifies infection but consider heat stroke and Ingestions Hypothermia may be caused by exposure or secondary due to adrenal failure, hypothyroidism, sepsis or drug/alcohol intoxication.

3. Rapid Neurological Exam: A 3-5 minute focused neurological exam will provide enough information to determine whether the cause of AMS/coma is metabolic or structural Level of Consciousness (GCS) – this is a useful index of the depth of impaired consciousness and is used for prognosis and communication amoung pre-hospital staff and trauma/neurosurgical consultants. GCS does not aid in diagnosing coma.

Cont--- GCS should be determined initially and repeated at regular intervals. A drop in the GCS score means a deteriorating condition and increased intracranial pressure secondary to an expanding mass lesion must be ruled out.

Table 1: Glasgow Coma Scale   EYE OPENING Spontaneous to voice to pain none Score 4 3 2 1

Cont--- VERBAL RESPONSE Appropriate, oriented Confused, disoriented Syllables, expletives Grunts None Score  5 4 3 2 1

Cont--- MOTOR RESPONSE Spontaneous, obeys commands Localizes pain Withdraws to pain Decorticate flexion Decerebrate extension None Score 6 5 4 3 2 1

Cont--- Head and Neck: Examine scalp for lacerations, contusions, deformities Signs of basal skull fracture (check tympanic membranes for CSF leak or hemotympanum , nares for CSF leak, “ racoon eyes” and “battle sign”) Flex neck if trauma has been ruled out to look for meningismus

Cont--- Motor and Sensory: Ask patient to move each limb or give painful stimulus; record best response and any asymmetry Painful stimuli include nail bed pressure and sternal pressure Check reflexes for asymmetry

Cont--- Cranial nerve exam: Check pupils for reaction and symmetry (with the exception of certain toxic syndromes, pupils are typically spared in metabolic and toxic syndromes) Extraocular movements (have patient follow a finger if awake enough, Doll’s eye maneuver if no trauma) Check fundi for papilledema (late sign of increase ICP)

Cont--- With rare exceptions, focal findings means a structural lesion. In particular, a dilated pupil on one side with weakness of the contralateral limbs indicates an expanding mass lesion on the side of the larger pupil.

Cont--- This occurs when the mass lesion is supratentorial and pushes or herniates the uncus of the temporal lobe through the tentorium (called “coning”). The oculomotor nerve, which runs adjacent to this, is compressed causing paralysis of the constrictor mechanism of the ipsilateral pupil.

4. General Examination: Feel the skin: warm, dry, diaphoretic Smell breath: can be a clue to cause of altered LOC Inspection/ skin exam: rashes (meningitis, sepsis), track marks, jaundice, evidence of trauma Examination of the lungs, heart and abdomen (masses, bowel sounds) may provide clues to other organ system disease .

5. Ancillary History: Obtained from family, friends, police, paramedics, old chart, etc. Onset and progression: abrupt onset suggests CNS hemorrhage/ischemia or cardiac etiology progression over hours/days suggests progressive CNS lesions or metabolic-toxic causes

Cont--- Preceeding events: patient’s baseline LOC preceeding deterioration antecedent trauma, fever, seizure activity Past medical history ( comorbities ie . COPD, cirrhosis, similar prior episode, mental health history, drug use)

6. Diagnostic Testing: The goal of diagnostic testing in a comatose patient is to identify treatable conditions (infection, metabolic abnormalities, seizure, intoxications/overdose, surgical lesions) Because neurologic recovery is reliant on early treatment, testing must proceed rapidly alongside, and in response to clinical evaluation.

Cont--- Examples of clinical clues which should prompt emergent diagnostic testing include: Papilledema or focal neurologic deficits suggesting a structural etiology require an emergent CT scan Fever suggesting bacterial meningitis or viral encephalitis mandates and urgent lumbar puncture and initiation of antibiotics

Management General Monitors, oxygen, vitals, IV access Airway management for declining GCS and inability to protect airway

Cont--- Antibiotics  for infection. Glucagon injection  for hypoglycemia. Intravenous fluids for dehydration. Naloxone  for narcotic overdose. Anxiolytics , or antipsychotics. Surgery to repair a hemorrhage or relieve pressure on your brain. Supplemental oxygen for hypoxia.

C LINICAL P EARLS Lumbar punctures in a comatose or AMS patient with focal findings should not be performed until an expanding mass lesion with increased intracranial pressure has been ruled out, as there is a risk of precipitating herniation of the brain stem through the tentorium .

Cont--- Other investigations include: Rapid blood sugar, CBC, electrolytes, Cr, BUN, LFT’s, glucose, serum osmolality , ABG’s, INR/PTT, troponin , urinalysis ECG, CXR, EEG electroencephalogram

DISPOSITION OF ALTERED MENTAL STATUS AND COMA: Patients with readily reversible causes of coma, such as insulin-induced hypoglycemia, may be discharged if treatment is initiated, the patient returns to baseline mental status, the cause of the episode is clear, and the patient has reliable home care and follow-up In all other cases, admission is warranted for further evaluation and treatment transfer patient if appropriate level of care not available

SUMMARY OF ALTERED MENTAL STATUS AND COMA: Causes of coma are diverse and include structural brain lesion and systemic disease; remember TIPS and AEIOU Stabilization of airway, breathing and circulation is the top priority; endotracheal intubation may be indicated to protect the airway Remember to maintain C-spine precautions in suspected trauma patients Dr. Adanwali

Cont--- Readily reversible causes such as hypoglycemia, hypoxia and opiate overdose should be considered (use universal antidotes “DON’T” as appropriate) Repeat GCS at regular intervals If elevated ICP is suspected, consult neurosurgery urgently If meningitis is suspected, initiate appropriate antibiotics immediately

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