approach to the patient with altered mental status...

Wolthers Laursen SA, Eberhard KE ©SATS Copenhagen | emss17.sats-kbh.dk

Approach to the patient with altered mental status

There are an enormous amount of differential diagnoses for altered mental status. This approach seeks to differentiate between diagnoses based on how fast they could cause death of the patient and how fast you are able to treat it.

Differential diagnoses that could cause death immediately:

! Airway obstruction ! Breathing (oxygenation) ! Cardiac arrest

1) A – airway, B – breathing, C – circulation: patent airway and vital parameters

2) Do not forget to obtain history from EMS, relatives or other witnesses

Differential diagnoses that could cause death the next few minutes:

! Hypoglycaemia ! Overdose ! Intracranial hypertension and incarceration

3) Blood glucose 4) Extended D – disability


5) E – exposure: Rapid top-to-toe 6) Differential diagnostic thoughts:

- Signs of impending incarceration: Hypertension, bradycardia, and irregular respirations (Cushing’s triad); posturing; unilateral blown pupil?

- Abdominal: Any sign of abdominal catastrophe, obvious pain or masses?

- Toxidrome: Vital signs, pupils, skin. - Trauma: Any clear signs of trauma?

7) Interventions: - If hypoglycaemia: Glucose IV - If (opioid) overdose: Naloxone - If signs of impending incarceration: Intubation; provide analgesia and

sedation; elevate the head of the bed; hyperventilation (to a target pCO2 of 35mmHg); Mannitol IV or 3% hypertonic saline IV.

Differential diagnoses that could cause death the next 10 minutes:

- ABCDEs - Hypotension - Anaphylaxis - Hyperkalaemia - Mitral insufficiency - Aortic disorders

ALTERED MENTAL STATUS

Signe Wolthers Laursen + Kristine E. Eberhard© SATS Copenhagen 2017 - emss17.sats-kbh.dk

ABCDE !! Be aware that patients with reduced !!conciousness might have a threatened airway

GCS - see pocket card

RESPIRATION: asses frequency and depth - Normal frequency and depth

- Depressed frequency and/or shallow depth - Abnormal frequency and/or depth

PUPILS: asses size, reflexes and symmetry- Normal size, normal light reflex, symmetrical

- Constriction, dilation, symmetrical/asymmetrical- No light reflex, symmetrical/asymmetrical

NECK STIFFNESS - asses flexion of the neck- Normal flexion- Neck stiffness

MOTOR FUNCTION: asses for lateralization and abnormal movements- Normal function and symmetry

- Lateralization- Pronation in upper extremity and extension in lower extremity (decortication)

- Flexion of upper and lower extremity (decerebration)

EYE MOVEMENT & BRAINSTEM REFLEXES: asses for deviation and spontaneous movements

- Normal without deviation and spontaneous eye movements- Deviation, symmetrical/asymmetrical

- Spontaneous eye movement

ADDITIONALLY: Check temperature, foetor ex ore, signs of trauma, needle marks, blood pressure and pulse


8) Remember re-evaluating ABCDE 9) ECG 10) Ultrasound: FAST and ECHO 11) Interventions:

- If hypotension: Fluid bolus or blood products. - If anaphylaxis: Epinephrine IM. - If hyperkalemia or abnormal ECG: Empirically calcium IV.

Differential diagnoses that could cause death the next few hours:

- Sepsis - Intracranial haemorrhagia - Alcohol withdrawal - Status epilepticus - Necrotizing fasciitis - Abdominal catastrophes - Metabolic (Diabetic ketoacidosis, hyponatremia, thyroid disorders and

adrenal disorders)


CEREBRAL ISCHEMIA INTRACEREBRAL HAEMORRHAGIA Definition Lack of perfusion due to thrombosis, embolus, thromboembolia

and hypoperfusion. Divided based on duration of symptoms: < 24 hrs. TCI and > 24 hrs. ischemic apoplexy.

Definition Spontaneous bleeding within the brain tissue resulting in intracerebral hematoma (ICH) often causing neurological deficits including unconsciousness. Divided in profound (basal ganglia) and lobar haemorrhagia. Causes can be divided in vascular and coagulopathies

Symptom and findings

Symptoms depend on the localization of ischemia. It is not possible to distinguish between hemorrhagic and ischemic causes based on symptoms. Neuroimaging is always acquired to differentiate. TCI is the only defined warning prior to ischemic apoplexy and should always be further examined. Smaller infarctions within the hemispheres do not compromise the consciousness. Infarction of the brainstem and infarction of the main cerebral arteries often cause decrease of consciousness. Occlusion of the main cerebral arteries will lead to neurological deficits. The medial cerebral artery is the most frequently affected artery, and it might lead to development of edema with possible herniation as consequence; a condition called malignant media infarction. ABCDE: Respiration can be compromised if the patient is unconscious (GCS > 9) or brainstem lesion. Neck stiffness: Not characteristically. GCS: Often decrease in GCS, but not always. Respiration: Nothing characteristically. Pupils: Pupil deficiencies can be present. Eye movement and brainstem reflexes: Conjugated eye deviation (head turned against the lesion). Motor function: Contralateral hemiformous paresis of face, arm and leg. Contralateral hemiformous lack of sensibility of face, arm and leg. Additional: Headache can be present Aphasia, problems speaking Neglect

Symptoms and findings

Symptoms depend on localization of the bleeding. Small hematomas rarely affect consciousness. Patients with less progressive hematomas will often suffer from slower progressing symptoms. Lesions above the brainstem often causes focal neurological deficits such as hemiparesis, hemianopsia ect. Brainstem lesions often leads to specific deficits. ABCDE: Respiration can be compromised due decrease in consciousness (GCS > 9) or brainstem lesion. Neck stiffness: Can be present, but not always and often 6-12 hrs. after bleeding. GCS: Often decrease in GCS, but not always. Respiration: Nothing characteristically. Pupils: Pupil deficiencies. Eye movement and brainstem reflexes: Conjugated eye deviation (head turned against the lesion). Motor function: Contrallateral hemiformous paresis of face, arm and leg. Contralateral hemiformous lack of sensibility of face, arm and leg. Additional: Acute severe headache Aphasia, problems speaking Neglect

Acute management

ABCDE. NB. exclude other pathology by CT/MR Thrombolysis (within 4.5 hour) Surgical approach: Intraarterial thrombolysis for patients with occlusion of main cerebral arteries. Decompressive craniectomy is considered in cases of malignant media infarction.

Acute management

ABCDE NB. exclude other pathology by CT/MR Symptomatic approach: reduction of hypertension (systolic blood pressure <160mmHg) Surgical approach: Evacuation of hematoma by craniotomy or endoscopy. In cases of hydrocephalus the treatment is a shunt.


TRAUMATIC BRAIN INJURY (TBI) TUMOR/METASTASIS Definition External mechanical cause of brain damage causing permanent or

temporary neurological deficits including unconsciousness. Is divided into 1) diffuse TBI (comotio) and the more severe diffuse injury with unconsciousness of >6-24 hrs. 2) focal TBI, is often localized in cortex and is often seen together with hematomas either in the epidural space, subdural space or sub arachnoidal space and skull fractures.

Definition Primary CNS tumors are derived from brain tissue, vessels or bone in relation to the nervous system. >95 pct. are intracranial (brain tissue) and 50 pct. are the types glioblastomes and astrocytomes. Secondary CNS tumors count metastases from cancer.


Symptoms depend on localization and severity of trauma from stabile to critical. Loss of consciousness, amnesia and symptoms of repeated vomiting are often present. ABCDE Neck stiffness: Can be present GCS: Mild TBI: 14-15, Intermediate TBI: 9-13, Severe TBI: 3-8. Respiration: Patients with severe TBI are in risk of hypoxia and should undergo endotracheal intubation on place of emergency. Pupils: asymmetrical size and loss of light reflexes can be present Eye movement and brainstem reflexes: Eye deviation can be present Motor respons: Depends on severity and varies from normal to decerebration.


All sorts of neurological symptoms can be present. Global symptoms due to the mass effect of tumor are headache, exhaustion, vertigo, dementia, nausea, confusion and affected consciousness. Depending on localization focal symptoms can be present. Irritative symptoms like epilepsy and focal motorical deficits can be seen as well. Edema around tumor might occur and cause symptoms of increased intracranial pressure (ICP). Due to the brainstem localization of tumors in children, and thus obstructive hydrocephalus (fluid accumulation in the brain), symptoms of increased ICP such as explosive vomiting and severe headache are often present. ABCDE Neck stiffness: No GCS, Respiration, Pupils, Eye movement and brainstem reflexes, Motor response: Nothing characteristically, depends on localization

Acute management

ABCDE Mild TBI (Low risk): GCS 14-15 !SB100 Mild TBI (intermediate risk): GCS 14-15 !CT/Hospitalization and observation >12 hrs. Mild TBI (High risk): GCS 14-15 !CT and observation > 24 hrs. Intermediate TBI: GCS 9-13 !CT and observation > 24 hrs. Severe TBI: GCS: 3-8 !Trauma centre and neurosurgery department. Depending on hematoma and mass lesion, surgical evacuation is necessary.

Acute management

ABCDE CT/MR/PET. Steroids are used to reduce the edema and thereby to ease symptoms. Before initiating steroids lymphoma and abscesses should be considered as differential diagnoses. Steroid in combination with antibiotics can be used in cases of cerebral abscesses. Signs of or pending herniation because of high ICP require acute intervention in order to decrease ICP. Mannitol and hyperventilation are medical options and acute tumor resection or shunt to avoid hydrocephalus counts the surgical approaches. Sub-acute treatment options depend on localization of tumor, comorbidity etc. Tumor resection, stereotactical biopsy, chemotherapy, radiotherapy and combinations are the established options.


MENINGITIS CONVULSIVE STATUS EPILEPTICUS

Inflammation of meninges, either bacterial or aseptic (viral, non-infectious) etiology.

Definition Continuous convulsive seizures > 5 minutes or recurrent seizures without neurological recovery. Status epilepticus can be non-convulsive as well.


SEPTIC MENINGITIS ABCDE: Depending on severity, everything from stable to critical Neck stiffness: Neck stiffness GCS: Reduced level of consciousness, confused Pupils: Not affected Eye movements and brainstem reflexes: Not affected Motor function: Not affected Additionally: Petechiae, fever, nausea, vomiting, photo-phono-phobia. Most frequent bacteria: pneumococcus, meningococcus, haemophilus influenzae. ASEPTIC MENINGITIS ABCDE: Depending on severity, everything from stable to critical Neck stiffness: Neck stiffness GCS: Rule of thumb - not affected Pupils: Not affected Eye movements and brainstem reflexes: Not affected Motor function: Not affected Additional: Milder symptoms and development over days, fever, nausea, vomiting, photo-phono-phobia. Most frequent virus: herpes simplex.


ABCDE: Depends on the duration of status epilepticus. After 30 minutes there is a high risk of cardiovascular collapse. You might find low saturation and lactate acidosis. Neurological deficits, low GCS score. Neck stiffness: Nothing characteristically GCS: Unconscious Pupils: Normal Eye movements and brainstem reflexes: Might find eye deviation Motor function: Convulsions Additional: Tongue biting, Feeling of déjà vu or jamais vu just before seizure, Head-turn Ask patient and relatives about the following to explore cause of status epilepticus: history of epilepsia, non-compliance of anti-epileptic medication, abstinence from alcohol or drugs, CNS infection, structural lesion (trauma, tumor), toxic/drug-induced.

Acute management

ABCDE Lumbar puncture Search for infection site: Examine and sample if possible from ears, sinuses throat, lungs, urine, blood. Order chest X-ray. Suspected bacterial meningitis:

IV Dexamethason IV Ceftriaxon IV Ampicillin Isolation until meningococcal meningitis is excluded

Acute management

ABCDE Treat reversible causes! 0-10 minutes:

Oxygen, IV access, ECG First 5-10 minutes: IV Diazepam Call anesthesia Blood samples: glucose, electrolytes, liver and kidney parameters. (If glucose < 3mmol/L, give IV Thiamine followed by IV 50% Glucose).

10-30 minutes: Repeat IV Diazepam IV Phosfenytoin (CAVE: patients heart conduction disease. Requires ECG and blood pressure monitoring!)

> 30 minutes: ICU and sedation CT cerebrum, EEG Lumbar puncture


ACUTE HYDROCEPHALUS TOXIC

Definition Enlarged ventricular system with increased intraventricular volume. Caused by a space-occupying process resulting in obstruction of third ventricle or the aqueduct or by an intracerebral heamorrhagia, shunt dysfunction, dysfunctional cerebrospinal fluid drainage, or structural abnormalities within fossa posterior.

Definition Unconsciousness due to use of opioids, alcohol, tricyclic antidepressant, neuroleptica and anticonvulsive medication, barbiturates, lithium, antidiabetics, insulin, methanol, benzodiazepines ect. The most common overdose outside the hospital is heroin (opioid).


ABCDE Neck stiffness: can be present, depending on reason to hydrocephalus, but normally it is not. GCS: Depends on severity. Respiration: Nothing characteristically Pupils: Papillary stasis. Eye movements and brainstem reflexes: Paresis of abducing muscle resulting in double vision. Adduction of eye in neutral position can be seen especially in children with increased intracranial pressure, but is not of focal diagnostic value. The sun set eye sign can be present, by which the eyes are driven downward. Motor function: Balance deficiencies and compromised ability to walk can be seen and fine motor skills can be affected as well. Additional: Acute severe headache and explosive vomiting. Cushing reflex/reaction = response to increased ICP that results in the triad of increased blood pressure, irregular breathing and bradycardia.


ABCDE Neck stiffness: Not characteristically. GCS: Level of consciousness varies. Respiration: Hypoventilation, eventually stop of respiration (opioids). Pupils: Pinpoint pupils (opioids), dilated/normal pupils can be present in case of prolonged overdose. Eye movement and brainstem reflexes: Nothing characteristically. Motor function: Overdose of benzodiazepines can cause symptoms like ataxia, lack of tonus, rigidity and tremble. Additional: Bradycardia and hypotension (opioids), pulmonary edema. Symptoms of withdrawal.

Acute management

ABCDE Eventually ophthalmoscopy. Acute external drainage or shunt. Causal treatment.

Acute management

ABCDE Opioid: Naloxone IV, Diazepam IV (convulsions), eventually gastric emptying and/or activated charcoal. Benzodiazepine: Flumazenil IV every minute until effect. Blood samples Urinary tests. Check limbs of stick marks.


KETOACIDOSIS WERNICKE’S ENCEPHALOPATI

Definition Condition defined by the presence of: 1) Blood ketone/3-hydroxybutyrat ≥ 3 mmol/l eller urinary ketone ≥ +2. 2) Metabolic acidosis (standard bicarbonate or total CO

2 < 18

mmol/l and/or pH < 7.30. 3) Hyperglycaemia.

Definition Caused by thiamine deficiency. Often seen in patients with chronic alcohol abuse and malabsorption. Petechial haemorrhages around the aqueduct in the brainstem. Administration of IV glucose possibly accentuate development in predisposed patients.


• ABCDE • Neck stiffness: Nothing characteristically • GCS: Often affected. The combined effect of hyperosmolarity of

plasma, dehydration and acidosis leads to increased osmolarity of brain cells and cerebral edema, which are expressed clinically by decreased consciousness.

• Respiration: Respiratory compensation of acidosis leads to hyperventilation or deep, heavy breathing (Kussmaul respiration)

• Pupils: Nothing characteristically • Eye movement and brainstem reflexes: Nothing characteristically • Motor function: Nothing characteristically. • • Additional: • Nausea and vomiting. • Fotor ex ore/breath smell: acetone. • Glycosuria.

Cerebral edema is an uncommon, but severe idiopathic complication. It might be related to fast decrease of blood glucose. The condition is often expressed when the biochemical situation seems to be stabilized.

•


ABCDE Neck stiffness: Nothing characteristically GCS: acute confusion or delirium Respiration: Nothing characteristically Pupils: Nothing characteristically

• Eye movement and brainstem reflexes: Paradox eye movements: nystagmus and double vision often due to bi- or unilateral paresis of abducens muscle.

• Motor function: Paradox motor function: explicit walk- and limp ataxia. Additional: Accompanying symptoms are agitation, hallucinations and confabulations. Characteristic abnormalities can be present within the mammilary corpus (brain structure) on MR.

Acute management

ABCDE Insulin (often 6 IE/hour) IV or subcutaneous. Fluid therapy. Antibiotics (focus of infection). If mentally different or decrease of consciousness, CT. If cerebral edema: Anti-edema therapy (mannitol and steroid).

Acute management

ABCDE On suspicion of Wernicke’s encephalopathy the treatment is injection of thiamine IV or IM (1-2 times per day in 7-10 days) and IV glucose before injection of thiamine is contraindicated!


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SUBARACHNOIDAL HAEMORRHAGIA (SAH)

Definition Arterial bleeding in the subarachnoidal space after rupture of intracranial aneurysma or due to Arterio-Venous malformation. Other causes are trauma, arterial dissection and amyloid angiopathy.


x ABCDE x Neck stiffness: Can be present (after 3-12 hrs. from ictus) x GCS: Often affected. Decreased consciousness. x Respiration: Respiration can be compromised due decrease in

consciousness (GCS < 9) or brainstem lesion. x Pupils: Can be affected. Often dilated, with no/little reaction to

light. x Eye movement and brainstem reflexes: uncoordinated eye

movements can be present, indicating lesion above brain stem. x Motor function: Depends on localization and size of

haemorrhage. Contralateral hemiformous paresis can be seen due to intracerebral hematoma.

x Additional: x Acute severe “thunderclap” headache/neck pain. Nausea and

vomiting. Increased ICP can be present: Cushing reflex/reaction results in the triad of increased blood pressure, irregular breathing and bradycardia. Complications are rebleeding, vasospasms and hydrocephalus. Acute headache as only symptom can be seen and are called a “warning leak”.

Acute management

ABCDE Always EXCLUDE SAH before any other differential diagnoses. Therefore: CT and CT angiography. If pathology is found on scan: Consult with neurosurgeon Keep patient fasting, vital parameters, neurological monitoring (GCS and pupils at minimum)

x Prophylactic therapies include: x IV calcium antagonist (nimodipin) x IV tranexamic acid x Symptoms of increased ICP: x Raise head of bed x IV mannitol/hypertonic saline

No visible pathology on CT: Lumbal puncture after 10-12 hrs. If bilirubin is positive (xanthocromia) Æconsult by neurosurgeon. If bilirubin negative: consider differential diagnoses (meningitis, migraine, encephalitis, hypertensive encephalopathy, apoplexia ect.) Neurosurgical evaluation of treatment options: either endovascular clips or conventional surgery clips of aneurism depending on localization etc. Eventually external ventricular drainage or shunt if symptoms of hydrocephalus are present.

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