As soon as a patient comes into into your examination room either from the OPD, the emergency room (ER) or from another clinic with a referral note you observe what the patient looks like. Why do you do this? What you see will determine how you treat this patient i.e. it will alter your behaviour.
- The patient is unconscious and is afebrile.
- The patient is unconscious with a high fever.
- The patient is unconscious and one arm and leg are flopping or stiff but not moving spontaneously.
- The patient appears in deep sleep, is not rousable, has been incontinent of urine, may have bitten his tongue and both plantars are upgoing.
- The patient is unconscious and has neck stiffness.
We will discuss most of these first.
There will be many more combinations which you will learn to recognize. This will help you start your diagnostic algorithm from a sensible point.
Let us deal with the unconscious patient first.
|Evaluation is essential.|
|Vital signs and general examination|
|Neurologic examination and GCS|
|Screening laboratories (CBC, glucose, electrolytes, BUN, creatinine, PT, PTT, ABG, LFTs, drug screen)|
|Head CT scan: prioritize emergent if focal neurologic signs, papilledema, fever|
|Lumbar puncture: prioritize emergent after CT scan if fever, elevated WBC, meningismus; otherwise do according to level of suspicion for diagnosis or if cause remains obscure|
|EEG: for possible nonconvulsive seizure, or if diagnosis remains obscure|
|Other laboratory tests: blood cultures, adrenal and thyroid tests, coagulation tests, carboxyhemoglobin, specific drug concentrations – do according to level of suspicion for diagnosis or if cause remains obscure|
|Brain MRI with DWI, if cause remains obscure|
|Intubate if GCS ≤8|
|Stabilize cervical spine|
|Blood pressure support as needed|
|Glucose 50 percent IV 50 mL (after blood drawn, before results back)|
|Thiamine 100 mg IV|
|Treat definite seizures with phenytoin or equivalent|
|Consider empiric treatments:|
|For possible infection:|
|Ceftriaxone and vancomycin|
|For possible ingestion of recreational drugs:|
|Gastric lavage/activated charcoal|
|For possible increased ICP:|
|For possible nonconvulsive status:|
|Phenytoin or equivalent|
The above chart is from version 6.0 of UpToDate database. It is taking into account that the patient who has been brought in unconscious presumably does not have a witness or caregiver accompanying him/her to the hospital. It is covering for
- meningitis; viral encephalitis: I would like to add cerebral malaria in Pakistan and India.
- stroke or intracranial bleed raised intracranial pressure.
- hepatic coma.
- drug overdose
- investigations aimed at other metabolic causes of a coma can be done once the common causes are ruled out.
As you get a history you can decide to do more tests or leave some out. How do you get a relevant history? Ask the person who brought the patient in, ask the paramedic who saw him first i.e the ambulance driver. See if the patient is wearing a medic alert bracelet or necklace. Look in the patient’s wallet: you may get an identity or the name of a person to contact; check the cell phone. In the owner’s own phone a name may be given and a number to contact in case of an emergency.
What do you do with the patient meanwhile?
Lay him down on a flat bed unless he is breathless; turn over to the left side preferably; clean the mouth; remove any dentures; suction the mouth; put in a plastic airway to pull the tongue forward and prevent the patient from choking on the tongue. Start oxygen at 2-4 litres /min by nasal prongs or a venti mask. Attach a pulse oximeter.
Check the pulse and BP. If the BP is low start IV saline and monitor the pulse and BP either with cardiometer which will also check the ECG or put a nurse on duty to check the pulse and BP 1/2 hourly. Apply a pulse oximeter. Do a 12 lead ECG and keep it in the record in the patient’s file. If the BP is falling add an infusion of dopamine or dobutamine.
As soon as a relative or friend becomes available clarify the following points:
- What was the time course of the loss of consciousness? Was it abrupt (eg, subarachnoid hemorrhage, seizure), gradual (eg, brain tumor), or fluctuating (eg, recurring seizures, subdural hematoma, metabolic encephalopathy)?
- Did focal signs or symptoms precede the loss of consciousness? As an example, an initial hemiparesis suggests a structural lesion, likely with mass effect. Transient visual symptoms (eg, diplopia or vertigo) suggest ischemia in the posterior circulation. Headache and vomiting just prior to loss of consciousness could indicate an intracranial hemorrhage.
- Did the patient have previous neurologic episodes that suggest transient ischemic attacks or seizures?
- What recent illness has the patient had? Has there been altered behavior or function recently? A fever suggests infection; an increasing headache suggests an expanding intracranial lesion, infection, or venous sinus thrombosis or an intracranial hemorrhage; recent falls raise the possibility of a subdural hematoma; recent confusion or delirium might indicate a metabolic or toxic cause.
- What prescription or nonprescription drugs are used? Are there medical or psychiatric conditions? Is there history of alcohol or drug abuse? Ask a reliable witness or caregiver.
- Speak to the patient’s doctor if possible.
Draw blood samples: blood complete picture, blood film for malaria parasites (in the tropics and subtropics), blood sugar and ketone bodies, electrolyte, BUN and creatinine, liver function tests (usually include bilirubin, alkaline phosphatase, ALT and serum albumin), arterial blood gases and pH of blood. In case you suspect infection (high fever, hypothermia, stiff neck, petechial hemorrhages, excessive sweating, a cardiac murmur) take a blood sample for culture. Find out what blood culture you current lab is using, ask for a bottle and also ask how much blood you should put in it. A few drops will get you a negative result, put 10 ml in an aerobic bottle and 10 ml in an anaerobic bottle, this constitutes a set. Approximately 3% for each ml of blood put into the media is the chance of picking up the causative organism. In adults, one blood culture set is rarely advisable or sufficient. A positive single culture result may not be interpretable unless an unequivocal pathogen is isolated. If a possible contaminant is reported on a single culture, additional culture data are needed, and in the interim, unnecessary antimicrobial therapy or unnecessary testing may be pursued. Take blood into two sets of culture bottles in adults one for aerobic and one for anaerobic culture.
A heart-beef infusion broth bottle, or gentian violet broth is commonly used used in Pakistan.
Special culture media may be helpful in the following settings:
- Use of blood culture bottles containing media with resins, lytic agents, or other neutralizing substances may be useful for documenting bacteremia in patients receiving antimicrobial therapy at the time blood cultures are obtained.
- Filamentous and dimorphic fungi, especially Histoplasma capsulatum, are best detected from blood with the centrifugation-lysis (Isolator) system, which is also useful in the detection of Mycobacterium avium and Mycobacterium tuberculosis.
- Special broth media (BACTEC) are also available for the detection of mycobacteria species.
- If you cannot get the samples to a lab within 1/2 an hour and if the weather is very hot, contaminants are likely to grow very fast and crowd out the pathogens. Please refrigerate but do not freeze your sample.
Do you need to do a lumbar puncture? If you are suspecting a space occupying lesion like a tumour or hematoma then do not risk the patient’s life. Likewise in a stroke or epilepsy or drug overdose do not do an LP. If you have managed to do a funduscopy and found papilloedema then do not do it. If you think this is an encephalitis or meningitis then the information obtained is very important and worth the risk from medullary coning. The latter can be prevented by taking no more than 5 ml of CSF with a thin needle and sealing it up immediately. and putting the patient in a head down position. If you are in the field or a facility where the CSF can neither be cultured nor examined under a microscope for cytology then do not do an LP.
Having taken the blood biochemistry samples start an IV infusion with normal saline. Giving 5% normal saline is like using 1/2 strength saline as the glucose metabolizes off or moves out of the blood rapidly. Using 5% glucose is even worse. The glucose is lost to blood and you are infusing just water into the blood and messing up the electrolyte and osmolarity. In a diabetic patient the glucometer will tell you at once what the capillary blood is; use insulin or IV glucose as indicated.
If there is a strong possibility of meningitis, encephalitis or cerebral malaria (include risk factors in your calculations like the endemic diseases in the area you are in, your knowledge of similar cases in or near the facility where you work, similar illnesses in families and contacts) start a combination of a broad spectrum antibiotic like ceftriaxone 2gm IV daily, acyclovir for herpes encephalitis 10 mg/kg IV 8 hourly and artemether or quinine.
Because acyclovir is only effective in halting viral replication, it should be given early, to prevent extensive replication and subsequent CNS damage. Early treatment is defined as any one of the following:
- Before loss of consciousness
- Within 24 hours of the onset of symptoms
- Glasgow Coma Scale score of 9 to 15
Early, aggressive antiviral therapy can prevent mortality and limit the severity of chronic postencephalitic behavioral and cognitive impairments. Acyclovir can be discontinued in 72 hours if the PCR result is negative for herpes simplex.
Antimalarial therapy — The risk of death due to severe malaria is greatest in the first 24 hours after clinical presentation.
Intravenous therapy should be initiated promptly, with close monitoring of parasite density. There are two major classes of drugs available for parenteral treatment of severe malaria: the artemisinin derivatives (artesunate and artemether) and the cinchona alkaloids (quinine and quinidine).
Patient weight <20 kg: IM, IV: 3 mg/kg/dose initially, followed by 3 mg/kg/dose at 12 hours, 24 hours, and 48 hours after the initial dose for a total of 4 doses over a period of 3 days. Transition to oral therapy at least 4 hours after the last dose of artesunate (WHO 2015).
Patient weight ≥20 kg: IM, IV: 2.4 mg/kg/dose initially, followed by 2.4 mg/kg/dose at 12 hours, 24 hours, and 48 hours after the initial dose for a total of 4 doses over a period of 3 days.
A single intramuscular dose in the above dosage may also be used. Patients who have received parenteral therapy for at least 24 hours and can tolerate oral medication may transition to an oral regimen for completion of therapy.
Quinine can be used as a slow IV infusion 600 mg every 8 hours for 3 to 7 days. An ECG and cardiac enzymes must be done at start of therapy and continuous cardiac monitoring is advisable. Note: Use in combination with tetracycline, doxycycline, or clindamycin. In South east asia the drug must be given for 7 days.
What else do you need to do?
Monitor the level of consciousness, vital signs, urine output and whether the drugs are being administered. Blood sugar needs to be monitored one hourly and the oxygen saturation in the blood continuously with a pulse oximeter. The urine output must be recorded adequately and balanced against the intake. Any urine output less than 20 ml must be noted, IV fluids given to improve hydration while carefully monitoring the central venous pressure (CVP). If the urine output does not improve and the hydration is clinically adequate then a challenge with IV dose of furosemide using 200-400 mg bolus to determine if the kidneys are responding. If the urine output does not increase then consider that the kidneys have shut down and restrict the fluid intake to output plus 500 ml in cool weather and 800 ml in hot weather. Cardiac arrhythmias must be watched for by using a cardiac monitor.
Reduce the intracranial pressure from rising or reduce it if already high. Cerebral perfusion pressure (CPP) is carefully kept constant when the intracranial pressure (ICP) is within 50-100 mm Hg. Conditions associated with elevated ICP, including mass lesions and hydrocephalus, can be associated with a reduction in CPP. Raised intracranial pressure makes the intracranial blood flow sensitive to even small changes and can cause focal or global ischemia. Patients with head trauma and a stroke are particularly susceptible. On the other hand, excessive elevation of CPP can lead to hypertensive encephalopathy and cerebral edema due to the eventual breakdown of autoregulation, particularly if the CPP is >120 mmHg. A higher level of CPP is tolerated in patients with chronic hypertension because the autoregulatory curve has shifted to the right. How do you recognize that the intracranial pressure is rising? If the patient is conscious he/she will complain of a headache which becomes worse. Look for “Cushing’s triad”. Signs include 6th nerve palsy, papilledema secondary to impaired axonal transport and congestion , spontaneous periorbital bruising and a triad of bradycardia, respiratory depression, and hypertension (Cushing’s triad, sometimes called Cushing’s reflex or Cushing’s response).
How do you prevent raised ICP?
Patients should be kept euvolemic and normo- to hyperosmolar. This can be achieved by avoiding all free water (including D5W, 0.45 percent (half normal) saline, and enteral free water) and employing only isotonic fluids (such as 0.9 percent (normal) saline). Serum osmolality should be kept >280 mOsm/L, and often is kept in the 295 to 305 mOsm/L range. Hyponatremia is common in the setting of elevated ICP, particularly in conjunction with subarachnoid hemorrhage. I am repeating this to emphasize it.
Sedate with propofol as it has a short half life and can be better regulated.
Blood pressure. Keep it above 60 mm Hg diastolic. Hypertension should generally only be treated when CPP >120 mmHg and ICP >20 mmHg.
Patients with elevated ICP have historically been positioned with the head elevated above the heart (usually 30 degrees) to increase venous outflow. It should be noted that head elevation may lower CPP; however, given the proven efficacy of head elevation in lowering ICP, most experts recommend raising the patient’s head as long as the CPP remains at an appropriate level.
Mannitol — Osmotic diuretics reduce brain volume by drawing free water out of the tissue and into the circulation, where it is excreted by the kidneys, thus dehydrating brain parenchyma. The most commonly used agent is mannitol. It is prepared as a 20 percent solution, and given as a bolus of 1 g/kg. Repeat dosing can be given at 0.25 to 0.5 g/kg as needed, generally every six to eight hours. Use of any osmotic agent should be carefully evaluated in patients with renal insufficiency.
Hypertonic saline bolus — With growing familiarity of use and accumulation of these data, hypertonic saline has increasingly been employed as a first line agent, supplanting mannitol at numerous institutions. Hypertonic saline in bolus doses can acutely lower ICP; however, the effect of this early intervention on long-term clinical outcomes remains unclear. The volume and tonicity of saline (7.2 to 23.4 percent) used in these reports have varied widely.
Furosemide, 0.5 to 1.0 mg/kg intravenously, may be given with mannitol to potentiate its effect. However, this effect can also exacerbate dehydration and hypokalemia
Glucocorticoids — Glucocorticoids were associated with a worse outcome in a large randomized clinical trial of their use in moderate to severe head injury.
Hyperventilation — Use of mechanical ventilation to lower PaCO2 to 26 to 30 mmHg has been shown to rapidly reduce ICP through vasoconstriction and a decrease in the volume of intracranial blood; a 1 mmHg change in PaCO2 is associated with a 3 percent change in CBF. Hyperventilation also results in respiratory alkalosis, which may buffer post-injury acidosis. The effect of hyperventilation on ICP is short-lived (1 to 24 hours) . Following therapeutic hyperventilation, the patient’s respiratory rate should be tapered back to normal over several hours to avoid a rebound effect .
Therapeutic hyperventilation should be considered as an urgent intervention when elevated ICP complicates cerebral edema, intracranial hemorrhage, and tumor. Hyperventilation should not be used on a chronic basis, regardless of the cause of increased ICP.
Barbiturates — The use of barbiturates is predicated on their ability to reduce brain metabolism and cerebral blood flow, thus lowering ICP and exerting a neuroprotective effect. Pentobarbital is generally used, with a loading dose of 5 to 20 mg/kg as a bolus, followed by 1 to 4 mg/kg per hr.
Therapeutic hypothermia — First reported as a treatment for brain injury in the 1950s, induced or therapeutic hypothermia has remained a controversial issue in the debate concerning the management of elevated ICP.
Removal of CSF — When hydrocephalus is identified, a ventriculostomy should be inserted. Rapid aspiration of CSF should be avoided because it may lead to obstruction of the catheter opening by brain tissue. Also, in patients with aneurysmal subarachnoid hemorrhage, abrupt lowering of the pressure differential across the aneurysm dome can precipitate recurrent hemorrhage.
Enteral and parenteral nutrition. Remember you need to feed the patient. The goal of nutritional support is to maintain lean body mass to prevent the negative consequences of protein malnutrition that can lead to multisystem organ dysfunction. Early institution of high-protein nutritional support is essential in the care of the injured or unconscious patient. Injured patients are susceptible to hypermetabolism, which leads to breakdown of skeletal protein and inhibition of protein synthesis. Pass a nasogastric tube if the patient is unconscious or cannot swallow. Meat broth, chicken broth, milk, yoghurt, soft eggs, jelly, custard and fresh fruit juice are recommended. commercial protein supplements like Ensure etc can be used.
Prevent aspiration pneumonia.
Essentially empty the stomach, if possible i.e. no raised ICP, keep the head down. If enteral feeding is started remember to keep the quantity of each feed not more than 200 ml at each session, empty out the stomach before putting in the fresh food as the previous food may not have emptied into the intestine and passive dilatation of the stomach may occur.
Prevent bedsores. Position the patient correctly, use an adequate mattress or surfacing material and change position of the patient frequently.
Position and inclination — The position and head inclination of bed-bound patients is likely to be important. It is recommended that:
- Pillows or foam wedges should be placed between the ankles and knees to avoid pressure at these sites when patients have no mobility at these areas.
- The heels require particular attention; pillows may be placed under the lower legs to elevate the heels, or special heel protectors can be used.
- Patients should be placed at an angle ≤30 degrees when lying on their side to avoid direct pressure over the greater trochanter or other bony prominences.
- The head of the bed should not be elevated more than 30 degrees to prevent sliding and friction injury.
Turning should be performed successively from the back, to one side, and then to the other side. The aim of repositioning is to reduce interface pressure and maintain microcirculation to areas at risk for pressure-induced skin and soft tissue injury. It is important that repositioning be done gently and properly, with the assistance of devices as necessary to avoid friction and shear forces. Timing and positioning should be documented