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Cardiac : VT !
Electrolyte : HyperNa, HypoNa, HyperCa
Encephalopathies
- Hypoxic encephalopathy
- Metabolic encephalopathy
- Hepatic encephalopathy
- Hypertensive encephalopathy
Thiamine : Wernicke’s encephalopathy
The goal of the physician is to rapidly determine if the CNS dysfunction
is from diffuse impairment of the brain
or if signs point to a focal (and perhaps surgically treatable) region of CNS dysfunction.
General category : diffuse CNS dysfunction (Toxic-metabolic coma)
or focal CNS dysfunction (structural coma).
A further division of structural coma into hemispheric (supratentorial)
or posterior fossa (infratentorial) coma
Abrupt onset suggests CNS hemorrhage/ischemia or cardiac cause.
Progression over hours to days suggests
progressive CNS lesion or toxic/metabolic cause.
Breathing pattern :
A variety of abnormal breathing patterns may be seen in the comatose patient.
They offer little information in the acute setting.
Abnormal extensor or flexor postures are nonspecific for localization
or cause of coma but suggest profound CNS dysfunction.
- Hyperthermia : Medication, Thyroid storm
- Hypothermia : Medication, Alcohol, Exposure, Sepsis, Hypothyroidism
- HTN : IICP
- Bradycardia : IICP, Cardiogenic, Hypothyrodism, Medication
大魔王
- CNS infection
- CO intoxication
- Encephalopathy
- Non-convulsive status epilepticus
- Endocrine, Vitamin
- Basilar artery thrombosis
BAO : in a comatose patient with “normal” results on head CT,
in which the only finding may be a hyperdense basilar artery
In nonconvulsive status epilepticus,
the patient is comatose or has fluctuating abnormal mental status or confusion,
but no overt seizure activity is present.
The diagnosis is challenging and is typically made by EEG.
Findings suggestive of nonconvulsive status epilepticus include
a prolonged postictal period after a generalized seizure;
subtle motor signs such as twitching, blinking, and eye deviation;
fluctuating alterations in mental status; or unexplained stupor and confusion.
Electrical seizures may continue in the absence of clinical seizures.
If the motor activity of the seizure stops
and the patient does not awaken within 30 minutes,
then consider nonconvulsive status epilepticus.
For children, consider ingestions, infections, and child abuse
in the appropriate clinical setting.
For IICP
A general recommendation is to keep the head elevated about 30 degrees
and at midline to aid in venous drainage.
Mannitol (0.5 to 1.0 gram/kg IV) can decrease intravascular volume
and brain water and may transiently reduce ICP.
Hypertonic saline infusion has also been found to be effective in reducing ICP.
In cases of brain edema associated with tumor,
dexamethasone, 10 milligrams IV, reduces edema over several hours.
Hyperventilation with reduction of partial pressure
of arterial carbon dioxide can reduce cerebral blood volume
and transiently lower ICP.
Current recommendations are to avoid excessive hyperventilation
(partial pressure of arterial carbon dioxide ≤35 mmHg)
during the first 24 hours after brain injury.
* What could kill my patient immediately ?
- Cardiac arrest
- Airway obstruction
- Breathing (Oxygenation)
Check pulse !
Vital signs
Airway patency and breathing pattern : Positioning, Oral/nasal airways, LMA
Taking history from surroundings
* What could kill my patient in the next few minutes ?
- Hypo G
- Overdose
- IICP
Neuro :
Pupils, Eye movements, Corneal reflex,
Moving all 4 extremities, Reflexes, Muscle tone, Any asymmetry ?
Signs of impending herniation :
HTN, Bradycardia, Irregular respirations (Cushing’s triad)
Posturing ; Unilateral blown pupil ?
Breathing pattern : Regular, Cheyne-Stokes, Irregular, Apnea
Toxidrome : Vital signs, Pupils, Skin
Signs of shock : Capillary refill, Skin warm or cold
Abdomen : Any obvious pain or masses
Trauma : Any clear signs of trauma
Hypoglycemia : D50W
Opioid toxidrome (or Suspicion) : Naloxone 0.2-0.4mg IV q2-3min.
(If the patient is stable, start with lower dose (0.04mg IV) to avoid precipitating rapid opioid withdrawal.)
Signs of impending herniation :
Intubate with analgesia and sedation
Elevated the head of the bed
Respirate to a target pCO2 of 35mmHg
Mannitol 0.5-1gram IV or 3% hypertonic saline 2-3ml/kg IV bolus.
* What could kill my patient in the next 10 minutes ?
- Still the ABCs
- Hypotension
- Anaphylaxis
- Hyperkalemia
- MI
- Aortic disasters
After the rapid primary survey and initial interventions,
I remind myself to reassess the ABCs.
If a rapidly reversible cause hasn’t been identified, I will start planning for a definitive airway.
ECG : Ischemia, Arrhythmia, Overdoses, and Hyperkalemia
Ultrasound : RUSH !
Any suspicion of anaphylaxis, I will give epinephrine 0.5mg IM.
If there is reason to suspect hyperkalemia, or bizarre appearing ECG : Empirically give calcium
* What could kill my patient over the next few hours ?
- Sepsis
- ICH
- Alcohol Withdrawal
- Status epilepticus (Presumably non-convulsive if I didn’t recognize it immediately)
- Necrotizing fasciitis (Look everywhere)
- Abdominal catastrophes
- Metabolic problems (DKA, HHS, HypoNa, Thyroid, Adrenal disorders)
Ensure the patient is adequately resuscitated before to the CT !
A definitive airway.
Any signs of shock are addressed with fluids, blood, and/or vasopressors.
Unless there is a clear alternative diagnosis, I start empiric antibiotics on everyone.
(Acyclovir can also be considered for herpes encephalitis.)
Non-convulsive status epilepticus is a difficult diagnosis to make.
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