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Syncope is a sudden loss of consciousness and postural tone followed by spontaneous, complete recovery. It is frequently related to inadequate supply of blood to the brain.
Likely etiology
Clinical clues to diagnosis
Vasovagal orneurally mediated syncope
Triggers: Prolonged standing or emotional distress, painful stimuli. Prodromal symptoms: nausea, warmth, diaphoresis
Situational syncope
Triggers: Cough, micturition, defecation
Orthostatic syncope
Postural changes in heart rate/blood pressure after standing suddenly
Aortic stenosis, HCM, anomalous coronary arteries
Syncope with exertion or during exercise
Ventricular arrhythmias
Prior history of CAD, MI, cardiomyopathy, or ↓ EF. Abrupt LOC with rapid recovery
Sick sinus syndrome, bradyarrhythmias, atrioventricular block
Sinus pauses, ↑ PR or ↑ QRS duration
Torsades de pointes(acquired long QT syndrome)
Hypokalemia, hypomagnesemia, medications causing ↑ QT interval
Congenital long QT syndrome
Family history of sudden death, ↑ QT interval, syncope with triggers (eg, exercise, startle, sleeping)
Seizures
sensory prodrome, incontinence, decrased consciousness, postictal
CAD = coronary artery disease; EF = ejection fraction; HCM = hypertrophic cardiomyopathy; MI = myocardial infarction.
The most important goal in the initial evaluation of syncope is risk stratification, which is determined through the history and physical exam, basic laboratories (hematocrit), and ECG.
A tilt-table test may used to confirm a diagnosis of vasovagal syncope if a diagnosis based on clinical examination is uncertain.
In patients presenting with a syncopal episode who have no history of congestive heart failure, a hematocrit > 30%, non-worrisome ECG, triage systolic blood pressure > 90 mm Hg, and no shortness of breath, the risk of an adverse outcome is relatively low, and further workup is probably not necessary.
Syncope treatment varies with etiology and seeks to prevent recurrence and reduce injury/death risk.
Midodrine, an alpha-1 agonist, can help treat neurocardiogenic syncope as well as syncope secondary to orthostatic hypotension.
Pacing is useful for some neurocardiogenic presentations (e.g. significant cardioinhibitory component or carotid hypersensitivity) and arrhythmic syncope.
An internal cardiac defibrillator is appropriate in patients with a documented uncorrectable ventricular tachycardia or an ejection fraction less than 35% without an arrhythmia.
Orthostatic or postural hypotension is a symptomatic fall in blood pressure following standing from a seated or supine position.
The etiology is either autonomic failure or volume depletion.
Autonomic failure is associated with an inadequate response of the neurohormonal mechanisms that increase vascular resistance and heart rate in response to postural change. Causes include:
Diabetes and associated neuropathy
Medication side effects of sympatholytics
Lewy body dementia
Aging, electrolyte disturbances, and infection
Acute volume depletion as caused by diuretic use, hemorrhage, or diarrhea/vomiting
Orthostatic hypotension is defined as a drop in systolic blood pressure greater than 20 mmHg when moving from lying down to standing. It is common in patients who are elderly, are hypovolemic, or have autonomic neuropathy (e.g., diabetes or Parkinson's disease). Additionally, medications such as diuretics, vasodilators, and adrenergic-blocking agents can cause orthostatic hypotension. Prolonged recumbence increases the risk. People will often note a pre-syncopal lightheaded sensation. The scenario described in this vignette is classic for orthostatic hypotension—an older person who experiences syncope upon standing after a period of bed rest.
To diagnose orthostatic hypotension, the patient is asked to rest in the supine position for five minutes. At the end of the five minutes, the patient is asked to stand and the blood pressure is taken. If one or more of the following drops in blood pressure are seen within 2-5 minutes of quiet standing, the patient can be diagnosed with orthostatic hypotension:
≥ 20 mmHg drop in systolic BP
≥ 10 mmHg drop in diastolic BP
Symptoms of cerebral hypoperfusion such as pre-syncope or syncope may be present.
Evaluation of a patient with documented orthostatic hypotension should include:
Detailed medication list including all OTC medications
Recent medical history of potential volume loss (vomiting, diarrhea, hemorrhage, fluid restriction)
Medical history of CHF, Diabetes, or Alcoholism
Physical examination evidence of neurologic dysfunction (parkinsonism, autonomic dysregulation as measured by abnormal pupil response, etc)
Management involves nonpharmacological and pharmacological interventions.
Non-phramacological interventions include:
Removal of offending medications
Maneuvers that decrease the drastic fall of BP upon standing(e.g. arising slowly, raising the head of the bed)
Increased salt and water intake
Pharmacological treatment of orthostatic (postural) hypotension:
Fludrocortisone is a synthetic mineralocorticoid that is first-line therapy for orthostatic hypotension
A sympathomimetic may be added if the patient remains symptomatic following therapy with fludrocortisone (pseudoephedrine, phenylephrine, and midodrine)
Other therapy utilized in combination (rarely as monotherapy) includes NSAIDs to decrease vasodilating effects of circulating prostaglandins and caffeine as a natural pressor.
Analysis of cerebrospinal fluid (CSF) is a common practice in neurology since many disease states have characteristic findings. Lumbar puncture (LP), or spinal tap, is the procedure used to obtain CSF.
In adults, the spinal cord extends to about L1, so the needle is generally inserted in the space between vertebra L3 and L4, which is even with the imaginary line that connects both iliac crests. This avoids the possibility of spinal cord damage.
In children, since the spinal cord extends lower, the needle is often inserted at lower levels between L4-L5 to L5-S1.
The needle passes through the skin, subcutaneous tissue, supraspinous ligament, interspinous ligament, ligamentum flavum, epidural space, dura mater, and arachnoid mater. Within the subarachnoid space is where the CSF is located. The needle has a hollow lumen through which CSF drains and is collected in multiple tubes for analysis.
The most common complication from a LP is headache. Remaining supine and oral fluids are often used to prevent these headaches, even though no study has found them to actually prevent or treat such headaches.
Nerve irritation from the needle can result in radiculopathies.
CT scans should be performed on patients with suspected increased intracranial pressure to avoid cerebral herniation, the most serious complication of LP. Patients with the following features should receive a CT scan before LP is performed:
Altered mental status
Focal neurologic defects
Papilledema
Seizure within the last week
Impaired cellular immunity
Note: Some emergency department will perform a CT scan on every patient prior to LP.
During a lumbar puncture initial gross appearance should be noted. Normal CSF should be colorless and clear.
A manometer can be used to measure the intracranial pressure.
Traumatic tap, in which the needle penetrates the epidural venous plexus, can cause CSF to look abnormal. This can be distinguished from blood in the CSF by collecting serial samples. The number of RBCs should decrease in successive tubes in the case of a traumatic tap.
There are a few classic formulas (groups of characteristics) that indicate a disease process.
Lumbar puncture in a patient with a bacterial infection will reveal:
WBC >50/mm3 with percentage of neutrophils greater than 80%
20-50 mg/mm3 glucose
100-250 mg/mm3 protein
May be culture positive
Increased ICP
Lumbar puncture in a patient with viral infection:
WBC 10-100/mm3 consisting of lymphocytes
Normal glucose
50-200 mg/mm3 protein
organisms may show when cultured
normal or slightly increased ICP
Lumbar puncture in a patient with fungal infection will reveal:
Decreased glucose
Elevated WBC count predominately lymphocytes
Increased protein levels
Elevated opening pressure
Lumbar puncture in a patient with a tuberculous infection will reveal:
WBC >25/mm3, predominantly lymphocytes
<50 mg/mm3 glucose
100-1000 mg/mm3 protein
PCR and special culture may show organism
Lumbar puncture in a patient with subarachnoid hemorrhage will reveal:
RBC >500/mm3
Normal glucose
60-150 mg/mm3 protein
Xanthochromia
Lumbar puncture in a patient with cerebral hemorrhage will reveal:
RBC 50-200/mm3
Normal glucose
50-150 mg/mm3 protein
Lumbar puncture in a patient with multiple sclerosis will reveal:
Normal or few WBCs
Normal glucose
Normal or slightly elevated protein
Oligoclonal bands
Lumbar puncture in a patient with meningeal cancer will reveal:
WBC 10-100/mm3
Normal or decreased glucose
Elevated protein
Neoplastic cells
Increased protein markers
Lumbar puncture in a patient with Guillain-Barre syndrome will reveal:
Increased protein
Normal pressure
Normal glucose
Normal white blood cell count.
Coma and stupor are clinical states in which patients are obtunded or unresponsive to external stimulation and are difficult to arouse or completely unarousable. The severity of a coma is graded by the Glasgow coma scale.
The ascending reticular activating system (ARAS) in the the upper pons and midbrain is believed to be integral to inducing and maintaining alertness. Any damage to this area can cause alterations in alertness within patients. Diffuse cortical injury can also cause a coma.
A patient who presents in a coma cannot contribute details of their own history. Therefore, it is important to ask questions to family and witnesses to determine the etiology of the coma. Common questions includes:
What was the time course of the loss of consciousness?
Any focal signs precede the loss of consciousness?
Does the patient have any history of neurologic episodes?
What medications is the patient taking?
Did the patient experience any trauma?
The first step in evaluation of a comatose patient is always airway, breathing circulation (ABCs). Once the patient is stable, further evaluation of the patient may begin in order to determine the etiology of the coma. A general examination of a coma patient should not be overlooked, as clues to the etiology of the coma may be found.
Vital signs may reveal hypertension, which can cause intracranial hemorrhage or hypertensive encephalopathy. A fever and hypotension may also be discovered indicating sepsis and circulatory collapse, leading to decreased perfusion to the brain.
Ventilatory pattern combined with blood gas is useful information to determine possible brainstem injuries, such as herniation. The shorter-cycle Cheyne-Stokes respiration is linked to brainstem tegmental dysfunction and may evolve into irregular respirations with the progression of downward herniation of the brain.
Evaluation of the skin and face for bruising may indicate head trauma. Needle tracks may indicate drugs use.
The neurologic examination of a comatose patient is brief and important to differentiate between structural or metabolic dysfunctions. The exam should focus on:
Level of consciousness
Motor response
Brainstem reflexes
Brainstem reflexes should be assessed for:
Pupillary light reflex
Corneal reflex
Eye movements (if patient is semi conscious)
The Glasgow coma scale (GCS) demonstrates responses in each of these areas which reflect the severity of the coma. The GCS is useful to determine the depth of impaired consciousness and for prognosis, but does not aid in the diagnosis of coma.
Motor examination for muscle tone and reflexes is important to determine any asymmetry, which will indicate a localized lesion to one side of the brain.
Patients with unprotected airways should be intubated. This usually is associated with a Glascow coma scale of ≤ 8.
Any hypotension is best treated with volume expanders or vasopressors. Hypertension should be treated with IV labetalol.
If a herniation syndrome is evident, immediate treatment with mannitol is recommended along with hyperventilation of the patient. These treatments reduce intracranial pressure associated with cerebral edema.
The GCS is obtained by adding the value for each category.
Minimum = 3
Maximum = 15
Typically a score of 8 or less will require intubation.
Score
Eye Opening
Verbal Response
Motor Response
1
None
None
No Movements
2
Open to painful stimulation
Incomprehensible sounds
Extends to pain
3
Open to voice
Inappropriate words
Abnormal flexion to pain
4
Open spontaneously
Confused, disoriented
Withdraws to pain
5
-
Oriented, converses
Localizes to painful stimulus
6
-
-
Obeys commands
Decorticate posturing consists of upper-extremity adduction and flexion at the elbows, wrists, and fingers, with lower-extremity extension. This occurs with dysfunction at the cerebral cortical level.
Decerebrate posturing consists of upper-extremity extension, adduction, and pronation together with lower-extremity extension. This occurs with dysfunction below the red nucleus, allowing the vestibulospinal tract to predominate.
Multifocal myoclonus, which are random, asynchronous muscle jerks in the limbs and trunk, suggests a metabolic or toxic etiology. Tremor and asterixis can suggest a metabolic encephalopathy.
Diagnosis of a comatose patient is focused on identifying a reversible underlying condition causing the coma. Investigations almost always include laboratory testing and neuroimaging. Some patients require lumbar puncture and electroencephalography (EEG).
Computed tomography (CT), allows for quick assessment of intracranial structural changes, and is usually the test of choice for the initial evaluation of a coma patient. It can determine underlying:
Tumors
Edema
Hydrocephalus
Intracranial bleeding
Magnetic resonance imaging (MRI) for detecting abnormalities in patients with:
Herpes simplex encephalitis,
Early ischemic strokes (especially involving the brainstem),
Multiple small hemorrhages or white matter tract disruption
However, it takes longer to obtain an MRI study and thus is not usually suitable for the unstable patient
Lumbar puncture is recommended in patients presenting with fevers. Cerebrospinal fluid analysis is important to rule out encephalitis and meningitis.
EEG is useful in comatose patients when an underlying seizure disorder is suspected.
Management of a comatose patient is focused on treating the underlying conditions and maintaining airway, breathing, and circulation.
