Case 1 scenario was on a comatose patient who presented with hyponatremia. This case will focus on management of coma with emphasis on the examination.

Clinical approach to a comatose patient

Prioritize as follows:

-Assess airway, breathing, circulation. Consider intubation if GCS< 8.

-Protect the cervical spine.

-Give 100% Oxygen, monitor pulse oximetry and obtain venous access.

-Record the GCS and check the  pupil size and reaction.

-Check the BM and the temperature.

-Consider the differential diagnosis.

-Look for a Medic Alert  bracelet  or necklace.                                      

Immediate therapy includes:

-If BM is low, give 50mL 50% dextrose i.v.

-If pupils are small, respiratory rate is low or signs of abuse are present, give 400 micrograms  naloxone i.v. stat, repeating the dose as necessary to a total of 1.2 mg if there is any suggestion of response. (! the half lives of most opiates are longer than that of naloxone, therefore repeated doses  or an infusion maybe necessary).

-IV thiamine if any suggestion of Wernicke’s encephalopathy.

-IV flumazanil for benzodiazepine intoxication if airway compromised.

-If hypothermic start rewarming. ( Important to note that any patient with prolonged immobility may develop: rhabdomyolosis, pressure necrosis, compartment syndromes and secondary hypothermia/sepsis).                  

Brief examination

- Vital signs are vital-obtain full set including temperature

- Signs of trauma.... haematoma, laceration, bruising, CSF/blood in nose or   ears, fracture ‘step’ deformity of skull, subcutaneous emphysema.

- Stigmata of other illnesses: liver disease, alcoholism, diabetes, myxodema. -Skin for  needle marks, cyanosis, pallor, rashes, poor tugor.  

- Smell the breath(alcohol, hepatic fetor, ketosis, uremia), meningism--but   do not move the neck unless cervical spine is cleared.                  

- Heart/lung exam for murmurs, rubs, wheeze, consolidation, collapse.

- Abdomen/rectal for organomegaly, ascites, bruising, peritonism, melanae.

- Are there any foci of infection(abscesses, bites, middle ear infection?)

- Any features of meningitis: neck stiffness, rash, focal neurology?

- Note the absence of signs, eg no pin point pupils in a kown herion addict, or a diabetic patient whose breath does not smell of acetone.

Check pupils every few minutes during the early stages, particularly if trauma is the likely cause. Doing so is the quickest way to find a localizing sign( so helpful in diagnosis, but remember that false localizing signs do occur)-and observing changes in pupil behavior (e.g. becoming fixed and dilated) is the quickest way of finding out just how bad things are.

Neurological evaluation 

The most important element in the evaluation of the comatose patient is obtaining a history from observers on the scene of the triggering event, from family members, and from emergency medical technicians who responded to the call for help. 

Find out the following:

- The circumstances in which the patient was found. Was there anything to suggest carbon monoxide poisoning? Were drug bottles or syringes near by? Was there a suicide note?

- When was the patient last seen?

- Is there a known past medical history, medication or allergies?

- Possible alcohol or drug use.                                                            

The coma examination then can be performed rapidly and can guide diagnostic testing and therapeutic measures. This is aimed at loctaing the pathology in one of two places. Altered level of consciousness implies either

( 1) a diffuse, bilateral, cortical dysfunction ( usually producing loss of awareness with normal arousal) or

(2) damage to the ascending reticular activating system (ARAS) located throughout the brainstem from the medulla to the thalami (usually producing loss of  arousal with unassessable awareness). 

The examination has four important components:

- Respiratory patterns

- Pupillary responses

- Eye movements

-Motor responses                                                                        

Respiratory pattern

Cheyne-Stokes breathing is a respiratory pattern that oscillates between hypoventilation and hyperventilation. It usually results from bilateral or diencephalic insult but may occur as a result of damage anywhere between the forebrain and the pons.                                    

Hyperventilation which may be due to acidosis, hypoxia or rarely, neurogenic. (Central neurogenic hyperventilation usually results from lesions of the central tegmentum of the pons, ventral to the aqueduct or the fourth ventricle. Patients breathe 40 to 70 times per minute. It is important to distinguish central neurogenic hyperventilation from pulmonary disorders. In general, central nervous system lesions cannot be blamed for hyperpnea if PO2 is less than 80 mm Hg or PCO2 is greater than 40 mm Hg.)

Apneustic breathing consists of a prolonged inspiratory gasp with a pause at end of inspiration, followed by expiration. Apneustic breathing is caused by lesions of the dorsolateral lower half of the pons .

Ataxic breathing is irregular in both rate and rhythm, is caused by medullary lesions, and usually is a preterminal pattern.

Pupillary responses

The brain- stem areas controlling consciousness are anatomically adjacent to those controlling the pupils and pupillary changes are a valuable guide to the presence and location of brain-stem pathology resulting in coma:

 -Normal direct and consensual=intact midbrain.

- Midposition(3-5mm) non-reactive +/- irregular=midbrain lesion.

- Unilateral dilated and unreactive (‘fixed’)=third nerve compression.

- Small,reactive=pontinelesion (‘pinpoint pontine pupils’) or drugs.

- Horners syndrome= ipsilateral lateral medulla or hypothalamus lesion,  may precede uncal herniation.

Eye movements - Almost all patients with ARAS pathology will have eye findings.

Observe resting position and spontaneous movement; then test the vestibulo-ocular reflex (VOR) with either the doll head manoeuvre (normal if the eyes keep looking at the same point in space when the head is quickly moved laterally or vertically) or ice water calorics ( normal if eyes deviate towards the cold ear with nystagmus to the other side.) If present, the VOR exonerates most of the brainstem from the VII nerve nucleus(medulla) to the third nerve (midbrain). Do not move the head unless the cervical spine is cleared, if spinal injury suspected do the ice water caloric test in which you irrigate the ear with 40-60mLs of ice water (first ascertain the integrity of the tympanic membrane ----can’t win can you? )

While we are on the eye we probably should mention fundi examination. Look for papilloedema, subhyaloid haemorrhage (These are large effusions of blood which have a crescentic shape and well marked borders that are visible on fundoscopy. They may be a sign of subarachnoid haemorrhage. May look like this-CLICK), hypertensive retinopathy, signs of other diseases.

Motor responses

It is important to observe the comatose patient for any spontaneous motor movements, which are always good prognostic signs. If the patient spontaneously moves only one side, a hemispheric or brainstem lesion is probably present contralateral to the side not moving. If there are no spontaneous movements, a noxious stimulus, such as nail bed or supraorbital pressure, should be applied.

Decorticate posturing (flexion at the elbow and wrist bilaterally, with shoulder adduction and extension of the legs) suggests a lesion above the brainstem, specifically above the red nucleus . Decerebrate posturing (internal rotation and adduction of the shoulder with extension at elbows, wrists, and legs) is usually associated with a bilateral midbrain or pontine lesion . This lesion is classically at the level of the red nucleus on the midbrain. Rarely, metabolic encephalopathies, such as hypoglycemia, may produce a similar picture. In general, decerebrate posturing has a worse prognosis than decorticate posturing.

Myoclonus consists of nonrhythmic jerking movements in single or multiple muscle groups and usually is associated with anoxic injuries (cortical reflex myoclonus) or metabolic encephalopathies, such as hepatic encephalopathy. Rhythmic myoclonus suggests brainstem injury.

Approach to investigation and Management

Investigations          

Immediately organize:

-FBC, U&Es, glucose, renal and liver function tests.

-Chest radiograph (aspiration?)

-ECG - beware ‘ischaemic’ changes in subarachnoid hemorrhage

-Sepsis screen (blood cultures; urine dipstick and M,C &S).

-Arterial blood gases.

-A CT or MRI scan of the brain will be required as an urgent investigation in any patient who is comatose for unknown reasons. (wishful investigation back home but at least we know about it).  This may reveal something that requires immediate neurosurgical attention, e.g. some extradural, subdural or intracerebral haematomas and all cases with these conditions should be discussed with a neurosurgeon.      

-A lumbar puncture will be required, after CT scan, in selected patients (Oh what luxury!)

Management

The following emergency measures are general requirements of the comatose patient:

-Protected airway.

-High-flow Oxygen.

-Intravenous fluids.

-Urinary catheter.

-Broad-spectrum antibiotics and/ or antivirals should be given empirically if there is any suggestion of bacterial infection or encephalitis.       

-Half- hourly neuro-observations

-A suitable pressure relieving mattress.

The patient’s resuscitation status must be considered and recorded when a specific diagnosis has been established and prognosis assessed.

Summary

Remember ABCs  first with immediate therapy. Brief history and examination to detect problems that you can correct immediately. Rapid neurological assessment is key to appropriate management, under it consider respiratory pattern, eye movement, pupillary response and motor response. And finally do not forget to take stock/ reassess.

The following link will give, I think, one of the best explanations to the whys and whens of evaluation of a comatose patient- CLICK HERE.

 

References

1.Oxford Handbook of Clinical Medicine

2.Medical Masterclass - Emergency medicine

3. Postgraduate Medicine vol III /no 2/February 2002