Decreased LOC: An Approach To Common Causes
• List structural and metabolic causes of decreased level of consciousness
• Identify key assessments to differentiate causes of decreased level of consciousness
• Discuss treatment of the undifferentiated unconscious patient
You are called to a shelter in the downtown core at 2 a.m. on a cold February evening for a 57-year-old man found unconscious in the rear alley. When you arrive police officers have secured the scene. You see no drug or alcohol paraphernalia.
The shelter manager tells you there is a strict curfew of midnight, and that the man, whom he knows well, often arrives back after midnight and sleeps in the alley until the doors open at 6 a.m. The manager says the man has many medical and psychiatric problems, but the shelter does not provide medications or healthcare.
Your partner is at the man’s head and reports he is protecting his own airway—no snoring or secretions—and breathing at a rate of 10, full, with a strong but irregular pulse at a rate of 55. He moans and withdraws to deep painful stimulus but does not open his eyes. His pupils are equal and reactive at 3 mm.
Some pertinent questions to consider:
1. What is this man’s GCS?
2. Which narcotics do not cause pupil constriction?
3. List 10 potential diagnoses for this patient’s altered level of consciousness.
4. How do you determine if the airway is patent?
Decreased Level of Consciousness
Consciousness is the awareness of one’s own self. It includes arousal (a scale from alert to comatose) and cognition (levels of awareness and orientation). The brain stem is responsible for arousal and is also sensitive to metabolic, toxic, and mechanical insults.
Causes of decreased level of consciousness are divided into two main categories: structural and metabolic. Structural abnormalities are anatomic events that affect the contents of the cranial space and include:
- Hemorrhage (epidural, subdural, subarachnoid, intraparenchymal)
- Clot (embolus, thrombus)
- Fluid (encephalopathy—hepatic, uremic, or high altitude; hydrocephalus)
- Infection (brain abscess, bacterial meningitis, viral encephalitis)
- Foreign body
More questions to consider:
5. Which two of the above conditions present with neck stiffness and photophobia?
6. What is the difference between an embolus and a thrombus?
7. Which type of intracranial hemorrhage is almost always secondary to trauma?
Metabolic abnormalities are often remembered using the AEIOU TIPS mnemonic. There are several variations of this mnemonic, many of which include structural causes. This version is for strictly nonstructural causes. The list is not exhaustive but meant to represent common causes that should be considered prehospitally.
- Alcohol and drugs—Ethanol and toxic alcohols (ethylene glycol, methanol); anticholinergics, opiates, barbiturates, benzodiazepines, anticonvulsants, antipsychotics; carbon monoxide, cyanide
- Electrolytes and endocrine abnormalities—Hyponatremia (low sodium), myxedema coma (hypothyroid), Addison’s crisis (low cortisol)
- Insulin (diabetic problems)—Diabetic ketoacidosis, hyperosmolar, hyperglycemic nonketotic states, hypoglycemia
- Oxygen levels low—Hypoxia secondary to respiratory or cardiac failure, pulmonary embolism, hypotension
- Temperature extremes (hypothermia, hyperthermia)
- Infection (sepsis, meningitis)
- Psychiatric conditions
- Seizure or postictal
8. What is the definition of sepsis?
9. What endocrine gland produces cortisol?
10. How does cyanide act as a poison?
Hallmark findings may lead prehospital providers to suspect a particular cause for each of the above conditions based on incident history, physical exam, field diagnostic tests, and medical background.
Back to the Case
The man in the alley requires a thorough trauma assessment to determine if he has signs of a head injury or internal bleeding. Assault or fall can’t be ruled out, necessitating a detailed thoracic and abdominal assessment.
An irregular heartbeat could indicate atrial fibrillation, increasing stroke risk in a man who’s not compliant with anticoagulation medication, and anticoagulation increases the risk of intracerebral bleeding. Motor assessment should indicate bilateral withdrawal to painful stimulus; unilateral findings would suggest cerebrovascular accident.
Following a trauma survey, you place the man on a stretcher in the warm and well-lit ambulance. Diagnostic tests reveal a blood pressure of 95/55 and a respiratory rate of 10, with 96% oxygen saturation on room air. His temperature is cold, atrial fibrillation is at a rate of 55 with no STEMI, and blood glucose is normal.
A detailed physical exam reveals the scent of alcohol on the man’s breath. A hematoma is felt beneath the hair on the right side of his head. His pupils remain equal and reactive, air entry is clear, and the abdomen is soft and not tender. You find no rash, no track marks, and no medical ID bracelet.
11. What are the diagnostic criteria for atrial fibrillation?
12. Why can atrial fibrillation cause a stroke?
13. Name the two organs in the abdomen most likely to cause significant bleeding in cases of abdominal trauma.
Supportive care of the ABCs is of the utmost importance until a definitive diagnosis can be determined.
Airway management may consist of manual maneuvers such as the head tilt and jaw thrust, which may improve ventilation and oxygenation. Attempt naso- and oropharyngeal lumens before intubation, as advanced airway management may be postponed until hospital arrival unless oxygenation can’t be maintained.
Should intubation be necessary in a patient with suspected increased intracranial pressure, it should be performed by the best operator with adequate sedation and analgesia to prevent spikes in cerebral pressure. Toxic exposures can cause both metabolic and respiratory abnormalities, so interpret end-tidal carbon dioxide readings with caution in potential toxic cases.
Use crystalloid fluids and vasopressors such as dopamine based on the suspected etiology of hypotension; shocks that are vasodilatory, such as septic shock, may benefit from both.
If available, tranexamic acid may be administered to patients with acute hemorrhage; the value of TXA in head-injured patients is still controversial.
Consider bypass to specialized centers for trauma, neurosurgical, cardiovascular, dialysis, stroke, and psychiatric conditions.
Treat hypoglycemia with glucagon or dextrose when a patient can’t orally consume carbohydrates. Opiate overdoses may be reversed with naloxone. Tricyclic antidepressant overdoses should be carefully monitored for ECG changes, at which point sodium bicarbonate should be administered.
Overdoses of calcium channel blockers and beta blockers may be treated with calcium and glucagon, respectively, in consultation with medical control. Other antidotes should not be used in polypharmacy overdoses without consulting medical control and poison experts.
Hyperkalemia (high potassium) can result from prolonged periods of immobility. Body pressure and hypoperfusion to tissue pressed against a floor, for example, can cause cell death, releasing toxins such as myoglobin and potassium into the bloodstream.
Signs of hyperkalemia on ECG include peaked T-waves, wide QRS, bradycardia, and sine wave. ECG changes in hyperkalemia are progressive and correlate to the level of potassium. Providers should understand and look for these changes. Take any of these signs seriously and consider treatment with intravenous calcium, inhaled beta agonists such as albuterol, and sodium bicarbonate. If both dextrose and insulin are available, they may be jointly administered to shift potassium into the cells.
14. Which poison will cause a falsely high SpO2 reading?
15. What is a normal end-tidal carbon dioxide reading?
16. Albuterol, calcium chloride, and sodium bicarbonate can all be used to treat which life-threatening electrolyte abnormality?
The Emergency Department
Upon arrival at the ED, the patient is intubated with etomidate, fentanyl, and rocuronium to secure his airway for transport to the CT scanner. A warming blanket is applied to raise his body temperature.
Cardiac, renal, liver, sepsis, and toxicology bloodwork are drawn. A chest x-ray shows large volumes consistent with COPD and a slightly enlarged heart. There is no evidence of pneumonia. The man is sent for a CT scan.
Bloodwork reveals increased creatinine, CK, and troponin, and a diagnosis of rhabdomyolysis is made secondary to nontraumatic crush injury. A complete blood count and blood cultures are normal.
The patient’s lactate is mildly elevated, labs are positive for ethanol and negative for drugs of abuse, and the liver panel is normal. Coagulation bloodwork is slightly elevated.
The CT scan shows a large right-sided subdural hemorrhage with no skull fracture. There is no evidence of ischemic stroke.
The man is flown to a neurosurgical hospital by a critical care helicopter crew; there he undergoes a craniotomy. He is discharged 11 days later.
What at first glance sounds like a very routine low-acuity call can in fact be a serious life-threatening emergency.
On close exam, this patient had head trauma, likely secondary to a fall from being intoxicated or possibly assault. Because of this he sustained a subdural hemorrhage that rendered him immobile on a cold night. He became hypothermic and suffered nontraumatic crush injury.
In people with alcoholism, brain atrophy increases the risk of subdural hemorrhage from delicate bridging veins, leading to bleeding that is often less dramatic than arterial bleeds in the epidural or subarachnoid space.
In patients with prolonged immobilization, nontraumatic crush injury can lead to rhabdomyolysis, acute kidney failure, hyperkalemia, and acidosis.
It is often easy to draw the wrong conclusions when faced with an unconscious patient; a drunk at a shelter can quickly be hauled to the hospital with little consideration for other pathology. In this case a careful examination and consideration of environmental, anatomic, and physiologic factors revealed a traumatic brain injury requiring neurosurgery, a life-threatening electrolyte imbalance requiring prehospital therapy, and hypothermia that could have contributed to coagulopathy and worsening intracranial hemorrhage.
Sidebar: Blood in the Brain
The Monro-Kellie hypothesis states that the brain is a closed space (the cranial vault) with a single outlet where the spinal cord exits. The vault has three contents: blood, brain, and cerebrospinal fluid (CSF). If the volume of one of these increases, the volume of the other two must decrease for pressure to stay the same.
As brain volume cannot change, CSF must be expelled from the vault through the spinal canal if blood accumulates. There are four types of bleeds that occur inside the cranial vault. A careful history and physical can often determine which type of bleed is most likely long before CT scans can be performed.
Epidural bleeds—Epidural bleeds are arterial and tend to be associated with a direct blow to the temple. The middle meningeal artery is the culprit in most cases; it rapidly pumps blood into the epidural space. The classic presentation is an initial loss of consciousness caused by the blow, followed by a period of lucid behavior, followed by deteriorating GCS as the blood accumulates and the brain is compressed.
Subdural bleeds—Subdural bleeds are venous in nature and often accumulate slowly, sometimes over a matter of weeks. They tend to bleed when stretched, as is the case where there has been brain atrophy followed by a good shaking. A textbook presentation would be a patient who is older or has alcoholism—both have slightly shrunken brains that can rattle around when the head shakes—with a history of falls. The trauma doesn’t necessarily have to be significant, as the smaller brain can tug at the veins and cause small, slow bleeds.
Subarachnoid bleeds—Subarachnoid bleeds are often arterial and caused by malformations or aneurysms that were pre-existing. They tend to affect middle-aged people and classically present as a “thunderclap” headache—a sudden, “worst-ever” headache. The blood irritates the meninges, and patients often complain of stiff necks, photophobia, and nausea. Hypertension is often witnessed before and after the bleeding begins.
Intraparenchymal bleeds—Finally, intraparenchymal bleeds, or intracerebral bleeds, occur inside the brain matter itself, beneath the pia mater. They can be caused by trauma, tumors, or hypertension. They often present similarly to an ischemic stroke in that a territory of the brain is disabled and focal neurologic deficits can be observed.
Obtain a thorough patient history in suspected cases of blood in the brain. Patients on antiplatelet medications such as ASA and clopidogrel and anticoagulant medications such as warfarin or dabigatran are at higher risk of bleeding. Afford additional clinical suspicion to patients on these medications who suffer head trauma. A CT is often warranted even in the absence of headache and neurologic deficit. And don’t forget to ask about blood thinners.
After a decade working as a helicopter paramedic, Blair Bigham, MD, MSc, EMT-P, completed medical school in Ontario, Canada, where he is now a resident physician in the emergency department. He has authored over 30 scientific articles, led major national projects to advance prehospital research, and participated in multiple collaboratives, including the Resuscitation Outcomes Consortium. E-mail him at firstname.lastname@example.org.