Alcohol Intoxication Mimics: ED DDx + Approach to Management
- Aug 30th, 2017
- Joe Bennett
Authors: Joe Bennett, MD (EM Resident Physician, NYU / Bellevue) and Hilary Fairbrother, MD, MPH (EM Attending Physician, NYU / Bellevue) // Edited by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)
A 58-year-old un-domiciled male with unknown past medical history presents brought in by EMS after bystanders found him unconscious on the sidewalk. EMS reports he was difficult to arouse.
Vitals: T 37.8, HR 102, BP 148/72, RR 16, SpO2 95% on room air
Exam is notable for somnolent male with poor hygiene. He has poor dentition and urine on his trousers. He does not awaken to voice, but groans and tries to swat you away when sternal rub is performed. There are no obvious signs of trauma and his abdomen is soft. You suspect alcohol intoxication and send an alcohol level to confirm your suspicions. Half an hour later, however, the lab reports the patient’s blood alcohol level as undetectable. Time to expand the differential.
Alcohol intoxication is the most common type of substance intoxication and abuse seen in the ED. Thirty percent of men and fifteen percent of women report at least one day of heavy drinking annually, and alcohol intoxication makes up about 2% of all ED visits in the US each year1. The CDC reports that the number of deaths due to alcoholic liver disease in 2014 was 19,388 and the number of alcohol-induced deaths, excluding accidents and homicides, was 30,7222. In total, it is estimated that 1 in 10 deaths in working-age adults may be attributed to excessive drinking3.
The legal limit of blood alcohol content set by the United States Department of Motor Vehicles (DMV) is 0.08%, but this number does not directly correlate to clinical intoxication. Individuals have baseline differences in alcohol tolerance which are then further impacted by rapid development of tolerance and dependence with chronic use. Alcohol intoxication therefore does not have any rigid definition, and is instead based on factors such as the ability to walk with steady gait, to adequately guard the airway, and to speak coherently without slurring words.
Alcohol is metabolized by the liver using alcohol dehydrogenase and aldehyde dehydrogenase through what are effectively zero order kinetics, meaning that alcohol is eliminated from the blood at a relatively steady state. Most adults metabolize 7-10g of alcohol per hour. This correlates to falls in blood alcohol content of roughly 15-20mg/dL/hr, although elimination rates can be as high as 30mg/dL/hr or more in chronic drinkers4. As such, most uncomplicated cases of alcohol intoxication require little more than monitoring and time to metabolize. Once clinically sober, most patients are able to walk out of the ED and return to their lives with no immediate consequences beyond perhaps a case of wicked veisalgia (hangover).
That said, alcohol intoxication can be quite challenging to manage in the ED. Presentations can vary dramatically and the differential diagnosis of apparent intoxication is broad, including almost any condition which can cause impaired cognition or altered mental status. Patients may present with simple slurring of words, aggressive or bizarre behavior, or be brought to the ED in an unresponsive state. History is often limited, co-ingestions are common, and the differential diagnosis includes some can’t-miss pathologies.
Let’s therefore discuss the different diagnoses that could be mistaken for simple alcohol intoxication.
Hypoglycemia occurs whenever blood glucose levels fall sufficiently low enough to cause clinical symptoms and risk of harm. Neuroglycopenic symptoms such as cognitive impairment, behavioral changes, somnolence, and even coma can closely mirror the clinical picture of alcohol intoxication. Immediately check a point-of-care (POC) blood glucose level for all patients presenting with suspected alcohol intoxication. Hopefully this is done at triage, but if not, it is on you to make sure it gets done.
If left uncorrected, hypoglycemia can result in significant brain injury and even death5. Alert patients may be given oral glucose. Both simple sugars and complex carbohydrates/fat/protein should be offered to the hypoglycemic patient able to safely tolerate PO (If you have this in your ED, you are better off than we are at Bellevue… one cheese sandwich please!). Patients unable to safely tolerate PO may be given IV glucose via administration of d10, d25, or d50. Caution should be used when administering d50, however, as it is strongly hyperosmolar and can cause necrosis if the IV infiltrates. D50 is also more likely than d10 to overshoot desired blood glucose levels and can potentially cause rebound hypoglycemia after administration.6 Glucagon can also be given and it opposes insulin and raises blood glucose levels by mobilizing the body’s endogenous glucose stores. Glucagon can be given IM, giving it particular utility for use in the case of the unconscious patient without established intravenous access. However, chronic alcoholics are likely to have dramatically reduced body stores of glycogen relative to healthy individuals, making glucagon less likely to be effective in the chronic inebriate.
Once identified and corrected, blood glucose levels should be monitored frequently and an investigation as to the cause of hypoglycemia should be performed. The majority of patients presenting with hypoglycemia are known diabetics. In the non-diabetic patient, the cause of hypoglycemia may be more difficult to identify. Sepsis, renal failure, hepatic failure, medications, prior gastric bypass, and autoimmune processes may all cause and potentiate hypoglycemia.
Alcohol abuse itself potentiates hypoglycemia and reduces the body’s ability to respond appropriately. Oxidation of ethanol leads to an excess of NADH relative to NAD. This causes a shift in redox potential which hinders the ability of cells to perform important oxidative processes such as gluconeogenesis4.
Traumatic Brain Injury
Patients with traumatic brain injury (TBI) may present with decreased cognition, confusion, somnolence, or unresponsiveness; all clinical pictures which are all easily mistakable for alcohol intoxication. The two also often occur in tandem, with alcohol use being a factor in at least 60% of TBIs7. For any patient suspected of having alcohol intoxication, it is therefore important to obtain whatever history is available from the patient, EMS, or bystanders as to whether or not the patient suffered any falls or trauma. On physical exam, look closely for signs of head trauma, particularly those suggesting skull fracture – Battle’s sign or raccoon eyes, CSF rhino/otorrhea, midface instability, or hemotympanum,
It is especially critical to identify TBI in patients with high blood alcohol content, as these patients have been shown to have increased in-hospital mortality compared to those with no alcohol on board – perhaps due to delayed identification or perhaps due to the impact of alcohol itself on the brain8.
If a patient suspected of alcohol intoxication presents with any head trauma, CT is the best initial imaging to obtain. While it may miss certain kinds of TBI such as diffuse axonal injury or cerebral contusions, it will readily identify those injuries which are amenable to emergent neurosurgical interventions – epidural hematomas, subdural hematomas, subarachnoid hemorrhage, or intraventricular hemorrhage.
Some stroke symptoms such as slurred speech, decreased cognition, altered gait, and depressed mental status can closely mimic the clinical picture of alcohol intoxication. This is mirrored by the fact that 2% of misdiagnosed CVAs are situations in which the patient is thought to be intoxicated with alcohol.9 This is another good reason to order a non-contrast head CT for patients with either unclear history, or for patients who do not appear to be appropriately metabolizing their presumed ingestion.
A practical rule of thumb is to re-evaluate a patient every hour who is thought to be intoxicated with alcohol. There should be a gradual return to baseline mental status, and if a patient is not approaching baseline mental status, a head CT and lab work (with alcohol level) should be considered. In every ED there is the potential to have patients lie in the corner for six hours waiting to metabolize, only to find out right before sign-out that their mental status hasn’t improved because they’re actually suffering from a large hemorrhagic stroke.
Other rules of thumb would be to always look at the pupils of a patient who is intoxicated and to check that patients with presumed intoxication are moving all extremities. These simple maneuvers may help you catch an otherwise easily missed CVA. Many times when we examine patients who are presumed to be intoxicated, we assume they are “asleep” and we do not open their eyes for an exam or prompt them to move.
Seizures are relatively common, with roughly 8-10% of the population experiencing a seizure at some point in their lifetime10 and seizures representing 1-2% of annual ED visits.11 The ictal phase of seizure is unlikely to be mistaken for alcohol intoxication, but the post-ictal period can closely mimic alcohol intoxication with confusion, slurred speech, and somnolence being common. Be sure to consider the diagnosis of seizure in any patient with a known seizure history, but keep in mind that one quarter of seizure presentations to the ED are first time seizures with no preceding history. The majority of post-ictal periods begin to improve within 10-20 mins. Be sure to reassess frequently and to revisit the differential if mental status does not improve as expected.
Seizures due to alcohol withdrawal are usually brief and often have extremely short post-ictal periods. Keep in mind that chronic alcoholics often live with elevated blood alcohol levels and thus can experience withdrawal (and withdrawal seizures!) while their blood alcohol levels remain significantly elevated. Seizures from alcohol withdrawal signify severe disease with high associated mortality. Alcohol withdrawal seizures warrant immediate and aggressive administration of benzodiazepines; preferably diazepam. These same patients may have altered benzodiazepine receptors and require massive doses (sometimes > 200mg of diazepam) to stave off further seizures.4
Encephalitis refers to any process causing inflammation of the brain. Viral infection (most common), bacterial infection (usually as a progression from preceding meningitis), or autoimmune disorder (such as anti-NMDA receptor encephalitis or Rasmussen encephalitis) are all potential etiologies. Early symptoms include headache, fever, aches in muscles or joints, fatigue, and weakness. Later symptoms include neurologic changes including slurred speech, confusion, weakness, sensory changes, agitation, hallucinations, and seizures. Presentation with these later symptoms could lead you to confuse encephalitis with acute alcohol intoxication.
Meningitis refers to inflammation of the meninges of the brain. Etiologies include:
Bacterial, viral, fungal, parasitic, neoplastic, autoimmune, traumatic, and drug induced. Patients with meningitis who are in late stages of the disease may present with symptoms easily confused with alcohol intoxication: altered mental status, abnormal gait, or post-ictal after having an associated seizure.
Knowledge of preceding illness, fever, or abnormalities on neuro exam may raise red flags that the patient presumed to be intoxicated may have a central nervous system infection. Again, a non-contrast head CT is a good first step – it may help distinguish these patients from those with simple alcohol intoxication, as CT (or MRI) may reveal signs of cerebral edema12. LP can sometimes identify the causative agent, although not always reliably13. EEG sometimes reveals characteristic patterns that may strongly suggest the diagnosis14.
One important way to avoid the infection vs. alcohol intoxication confusion is to make sure that all altered patients have an accurate temperature measured. Axial and peripheral temperatures are often measured on patients who are thought to be intoxicated, but can often report falsely normal temperatures on febrile patients. Make sure to lay (gloved!) hands on all of your intoxicated patients and to get a rectal temperature if your patient feels warm or has unexplained tachycardia.
Advanced sepsis can present with somnolence or depressed mental status, which can be confused for alcohol intoxication, particularly if the patient is a known chronic alcohol abuser. It should be remembered however, that chronic alcohol abuse depresses the immune system and increases the risk of certain infections such as aspiration pneumonia and cellulitis.
Sepsis should be readily identified by the presence of abnormal vital signs and signs/symptoms of infection. A full physical exam should be performed including full skin exposure to look for the source. That said, let’s stop and be honest for a moment… are any of us taking off all of the clothes of every well-known chronic inebriate every time they present to the ED? Again, it is important to be highly suspicious in these patients and to never ignore abnormal vitals. If you hear a junky cough or if despite sobering up a patient remains tachycardic… go back and take a second look. If a well-known chronic inebriate comes in and swears that they haven’t been drinking… take a second look. Fully undress them and do a full exam if you didn’t initially. Consider lab tests including a lactate and a venous blood gas. If a fever is noted, a chest x-ray and urinalysis may well be warranted as well. Take particular caution with cirrhotic patients, as they are extremely prone to infection and can worsen quickly (particularly with SBP).
Lactate levels are commonly used as a marker for severity of illness in sepsis. Keep in mind, however, that mild elevations of lactate are common in patient with severe alcohol abuse. Alcohol hinders the liver’s ability to process lactate, both through direct hepatic injury as in cirrhosis, and via generations of increased NADH/NAD+ ratio. An isolated elevation in lactate should therefore not be mistaken for sepsis without the presence of abnormal vitals or signs of infection. However it is worth noting that increased blood lactate levels from alcohol abuse rarely exceed 3mmol/L.15
Worsening kidney function usually produces no symptoms initially. However, as renal function declines patients can present with a wide range of symptoms including fluid overload, malaise, nausea/vomiting, pericarditis, pericardial effusion, and peripheral or CNS abnormalities including neuropathy, confusion, somnolence, seizures, or coma. These symptoms do not follow a clear progression and different patients will experience different symptoms at widely varying blood urea nitrogen (BUN) levels.
Suspect uremia in any patient with known history of CKD. Clues on physical exam include signs of volume overload (JVD, lower extremity edema, pulmonary edema, distended abdomen), HTN, and presence of a dialysis shunt or fistula. Labs will reveal elevated BUN and creatinine. Hyperkalemia and acidemia will also likely be present.
By the point that a patient is manifesting symptoms which would be mistaken for alcohol intoxication they typically have uremic encephalopathy and warrant urgent dialysis. Consult renal specialists early and assess for other life threatening complications of renal failure (acidemia, electrolyte abnormalities, fluid overload, pericardial effusion/tamponade, GI bleeding).16
Patients with hepatic encephalopathy can present with varying degrees of cognitive impairment ranging from altered sleep cycles to somnolence and coma. Suspect hepatic encephalopathy in any patient with known liver disease, particularly if they have had a recent TIPS procedure. Take a moment to look for sequelae of liver disease on physical exam: jaundice, scleral icterus, spider angiomata, caput medusae, lower extremity edema, firm/palpable liver, ascites, pruritus, palmar erythema, gynecomastia, significant bruising, asterixis.
There are, unfortunately, no measurable blood levels, imaging studies, or criteria to reliably diagnose hepatic encephalopathy. Rather, the diagnosis is clinical and inferred from the presence of altered mentation in the setting of hepatic dysfunction. Elevated ammonia levels are suggestive, but not diagnostic.17
Should you suspect hepatic encephalopathy, be sure to assess for GIB as this can often trigger decompensation and encephalopathy in cirrhotic patients and often represents a medical emergency unto itself. Cirrhotic patients commonly have underlying coagulopathies and varices, making GIBs potentially being complex and severe.
HIV encephalopathy refers to cognitive changes thought to be the direct impact of HIV infection as it disseminates throughout the CNS of infected individuals. The pathophysiology is poorly understood, but may be due to invasion of CNS macrophages and glial cells. The incidence of this disease has dramatically decreased in the era of widespread antiretroviral therapy, but may remain prominent in areas where patients do not have ready access to these drugs.18
Suspect this diagnosis in any HIV+ patient who presents in an altered state if they are not on ART or have a low CD4 count. These patients present with varying degrees of behavioral changes, motor symptoms, and cognitive impairment. Physical exam will likely show delayed cognitive speed with tasks such as addition and subtraction. Neuro exam may reveal alterations in saccadic eye movements, disjointed limb movements, dysdiadochokinesia, and hyperreflexia. CSF typically exhibits a high viral load and elevated protein, although these findings are not independently diagnostic.19 Cortical atrophy will likely be present on CT or MRI, if obtained.
Management relies on initiation of ART to increase CD4 count and reduce viral load.20, 21 Be sure to investigate closely for other HIV related causes of AMS such as opportunistic infections or CNS malignancy.
This form of encephalopathy occurs as a complication of thiamine deficiency, usually in the setting of chronic alcohol abuse and malnutrition. The classic triad of Wernicke encephalopathy is opthalmoplegia, ataxia, and confusion. However hearing and vision changes, lethargy, dysphagia, memory impairment, polyneuropathy, and hypothermia have all been reported.4
Wernicke’s is a difficult disease to recognize and the abnormalities on ocular exam are likely to be the best tip off. MRI classically shows changes in the mammillary bodies, although changes in the thalami and periventricular spaces are also often seen.22 Treatment includes thiamine supplementation and regular dosing of thiamine can help prevent this disease in high risk patients. Give thiamine IV or IM, as the GI tract of chronic alcohol abusers is unlikely to absorb orally administered thiamine efficiently. Many ED physicians habitually give thiamine 100mg IM to any chronic alcoholic seen in the ED. Doing so can save your frequent fliers from suffering from this disease.
Ingestions of many substances other than alcohol can closely mimic alcohol intoxication, and it is important to remember that co-ingestions are common. A positive alcohol level does not rule out use of other substances. Management of ABCs, consideration of gastric decontamination, hydration with crystalloids, and early involvement of a poison control center are central to the management of any suspected toxic ingestion.
Benzodiazepines – cause a very similar form of intoxication with slurred speech, ataxia, and depressed mental status. Intoxication of benzos alone is rarely life threatening, but when co-ingested with alcohol can lead to significant respiratory depression or airway compromise.4
Barbiturates – more rare since the widespread use of benzodiazepines. Barbiturate intoxication causes significant CNS depression more pronounced than that of alcohol or benzodiazepines4, and thus is more likely to require airway intervention.
Zolpidem (Ambien) – synthetic sleep aid which binds to benzo receptors and can produce similar symptoms.4 Managed with supportive care.
Gamma-hydroxybutyrate (GHB) – CNS depressant and recreational drug. In overdose, may present with profound hypotension, bradycardia, respiratory depression, and hypothermia. Treatment is supportive.23
Toxic alcohols (Methanol, isopropyl alcohol, ethylene glycol) – may present in almost identical fashion to alcohol intoxication, although blindness is a unique finding in late stages of methanol intoxication. Alcoholics may intentionally ingest methanol and other patients may accidentally ingest methanol in home-made alcohols such as moonshine. Labs will show significant metabolic acidosis, elevations in lactate, and an osmolar gap. Treatment involves administration of bicarb, inhibition of alcohol dehydrogenase with fomepizole or ethyl alcohol, and emergent dialysis in severe cases.4
Isoniazid (INH) – acute toxicity can present with depressed mental status, coma, or seizures. Symptoms are due to deficiencies in Vit B6 and GABA. Treatment centers on the prevention of seizures, and administration of pyridoxine (vitamin B6). Use of bicarb is controversial and hemodialysis is rarely performed.4
Lithium – neurologic sequelae of lithium toxicity tend to occur well after other symptoms classic of lithium toxicity have presented. Nausea, vomiting, diarrhea, and cardiac dysrhythmias will likely have preceded neurologic changes. Patients are often volume depleted secondary to diabetes insipidus.4
Opioids – patients tend to present somnolent with depressed respiratory drive. Pinpoint pupils are characteristic on exam. Naloxone may be given, but only in doses sufficient to maintain respiratory drive (no need to throw a patient into withdrawal!).4 Recently we have seen synthetic opioid street drugs that cause profound respiratory depression and arrest, and require massive doses of naloxone for reversal.
Electrolyte imbalance (hypo/hypernatremia, hypercalcemia)
Multiple electrolyte imbalances can present with somnolence or altered levels of consciousness; in particular hypo- or hypernatremia and hypercalcemia.
Hyponatremia has multiple etiologies, and patients may be hypo-, eu-, or hyper-volemic depending on the cause. Regardless of the etiology, by the time hyponatremia causes alterations in mental status it is likely to be severe. Hyponatremia should be corrected as slowly as possible, but in the case of the patient with altered mental status more rapid correction is usually warranted via administration of hypertonic saline (starting dose of 100mL of 3% NS generally recommended).24 Bear in mind that hyponatremia is one of the most common electrolyte abnormalities encountered in chronic alcoholics, so be on the lookout for this pathology when they come in.
Hypernatremia results usually from dehydration; loss of fluids without concomitant loss of sodium. By the time hypernatremia causes altered mental status, there will usually be obvious signs of hypovolemia which respond well to administration of dilute fluids to replace free water deficits.25
Hypercalcemia presents with mental fogginess, with patients often speaking slowly and appearing somnolent. Constipation, nausea, diffuse weakness, and fatigue will likely be present. Suspect this diagnosis in patients with known malignancy, as hypercalcemia of malignancy tends to cause more rapid increases and greater concentrations than are encountered in other causes.26
DKA and HHS can present with somnolence and altered mental status. These diagnoses should be suspected in any patient with an elevated initial POC glucose reading is significantly elevated (another good reason to check POC glucose on arrival). Patients will likely have signs of dehydration (such as dry mucous membranes) and may have Kussmaul breathing patterns. Urine will reveal ketones in the case of DKA, but not in HHS. A venous blood gas may show profound acidemia.
Hypothyroidism / Myxedema coma
As severe hypothyroidism progresses to myxedema coma, patients may present with varying degrees of altered mental status and impaired cognition. Patients may also be hypothermic, bradycardic, hypotensive, and have decreased respiratory drive. Look for non-pitting edema of the hands, face, or tongue (the myxedema part of myxedema coma) and look for any scars to indicate thyroid surgery.
Labs may show hyponatremia and hypoglycemia. TSH may be low, normal, or high depending on the etiology, but T3 and T4 levels will be low. The condition carries high mortality and warrants emergent treatment. 27
Hypothermia may be present in a multitude of conditions which can result in altered mental status (sepsis, toxic ingestions, hypothyroidism, etc.). Be sure to assess for these conditions before assuming hypothermia is due to exposure alone. Regardless, hypothermia should always raise a red flag that your patient is likely on the sicker end of the spectrum.
Mild hypothermia due to exposure can present with slurring of speech, while moderate/severe cases can present in somnolent or comatose state. The condition should be readily identified when triage vitals are taken and apparent on physical exam. Be sure to obtain a core temperature, but be cautious in using core temperatures during the rewarming process, as rectal and bladder temperatures may lag behind the rest of the body and result in overshooting temperature goals. Be sure to fully undress patients to look for signs of frostbite or trauma. Obtain an ECG and monitor closely for any electrolyte abnormalities as these are common.28
Severe hypotension can result from fluid shifts during rewarming, so aggressive fluid resuscitation and the use of pressors may be warranted. Electrolyte disturbances and rhabdomyolysis may also occur.29
And now the really rare presentations…
B12 deficiency can result in ataxia and mental status changes that can be mistaken for acute alcohol intoxication. By the time these symptoms develop, however, significant macrocytic anemia is likely to be present and may help clue you in to the appropriate diagnosis. Keep in mind that chronic alcoholics are classically malnourished and thus more likely to suffer vitamin deficiencies (B12 and folic acid) than other patients. Macrocytic anemia is most likely caused by folic acid deficiency in these patients30, but remember to keep B12 deficiency on the differential.
MS may present with dysarthria, gait abnormalities, and impaired cognition. The symptoms, while potentially acute, are usually relapsing/remitting in nature. Diagnosis rests on identification of other signs and symptoms such as spasticity, changes in sensation, bowel or bladder dysfunction, inter-nuclear ophthalmoplegia, pendular nystagmus, pain, vertigo, or visual loss. Identification of CNS lesions which have occurred on multiple instances, separated by time and space, is the key to accurate diagnosis. MRI will likely reveal cerebral or spinal plaques which support the diagnosis, but are not independently diagnostic.31
Wilson disease is a rare disorder resulting from genetic abnormalities in cellular copper transportation. Symptoms usually present between the ages 5 and 35, with a wide array of potential presenting symptoms. Gait abnormalities, slurred speech, and cognitive impairments are common presenting symptoms which could easily be mistaken for alcohol intoxication.
The combination of psychiatric disease, liver disease, and neurological symptoms should raise concern for Wilson disease. Physical exam may reveal tremor, dystonia, chorea, myoclonus, hyperreflexia, hepatomegaly, liver disease sequelae, and characteristic Kayser-Fleischer rings on the eyes.32
This syndrome is caused by excess corticosteroids in the body, either by exogenous administration or from increased endogenous production. Less commonly, Cushing syndrome can present with cognitive impairments, which may be mistaken for alcohol intoxication. A history of long term steroid use (as in SLE or rheumatoid arthritis) should raise concern for the diagnosis and prompt further investigation.
Treatment centers on identification and correction of underlying causes.33 Beyond holding any steroids being given, there is little in the way of ED treatment for this disease. Consider admission if the patient is unwell appearing, but otherwise referral to endocrine specialist is reasonable disposition.
Symptoms of adrenal insufficiency manifest as a result of critically low corticosteroid levels within the body. Systemic symptoms such as fatigue, muscle aches, nausea, abdominal pain, lethargy, fever, confusion, or coma are common presenting symptoms, and will progress to shock if not addressed in timely fashion. By the time patients present with decreased cognition or altered mental status, they are likely to be in the more severe stages of the disease.
Diagnosis can be difficult given the nonspecific symptomatology, but the presence of hyper- or hypopigmentation of skin on physical exam may give a clue as to the underlying pathology. If history can be obtained, it may reveal systemic symptoms as above preceding the decline in cognition and mental status. Electrolyte abnormalities are common, with hyponatremia and hyperkalemia being the most characteristic. Hypoglycemia and hypercalcemia may also be present.34 With these being the most common electrolyte abnormalities in chronic alcohol abuse, it is not difficult to see why this rare diagnosis is often missed in the ED.
Management involves administration of stress dose corticosteroids, management of electrolyte imbalances, and supportive care.
Hypoxia / hypercarbia
Both hypoxia and hypercarbia can present with somnolence and altered mental status. Hypoxia can be readily identified by pulse oximetry and therefore is rarely missed after patient triage. Hypercarbia is measured by arterial, capillary, or venous blood gas analysis and can be much more subtle in its presentation. Hyper- or hypoventilation may be present. Have a heightened suspicion for hypercarbia in any patient with known history of COPD, asthma, or other pulmonary pathology. Treatment includes optimization of oxygen and ventilation through supplemental oxygen and respiratory support with non-invasive or invasive ventilation.
Carbon monoxide (CO) poisoning can cause symptoms ranging from headache to lethargy and coma. Suspect CO poisoning during winter months, particularly if multiple people from the same family present with similar symptoms.
Diagnosis is made via co-oximetry (usually from an arterial blood gas sample). Treatment includes oxygen supplementation and hyperbaric oxygen, which are both warranted by the time a patient appears altered from a CO exposure.35
Dementia is a catch-all term used to describe any cause of steady cognitive decline not due to delirium or acute illness. Patients suffering dementia can present with cognitive impairments, slurred speech, and bizarre behavior, which could be mistaken for intoxication if there is no knowledge of the patient’s history. Suspect dementia in patients whose symptoms who do not improve over the course of hours but keep in mind that this a diagnosis of exclusion. Attempt to find other family members and friends to confirm the patient’s baseline mental status.
In the end, it isn’t our job to diagnose dementia in the ED. Our job is rather to rule out the more dangerous possible causes of the symptoms above.
Psychiatric disease can manifest in numerous ways, many of which may involve altered cognition. Negative symptoms of schizophrenia or severe depression may present with apparent somnolence. These disorders should be suspected in patients with known history, odd affect, or poor self-care. Focus on controlling any dangerous behavior, assessing for any suicidal or homicidal ideation, and ruling out any potentially dangerous organic causes for the symptoms. As with dementia, it isn’t our place to diagnose psychiatric disease in the ED. Psychiatric evaluation is warranted only after dangerous organic causes have been considered and ruled out.
Take Home Points
– Keep a broad differential in mind for any patient with AMS, even if the patient smells like alcohol and intoxication seems likely
– Check a POC blood glucose level on arrival
– Undress patients suspected of alcohol intoxication and fully examine
– Re-assess every 1-2 hours. If your patient doesn’t improve as expected, reexamine and broaden the differential
– Don’t ignore abnormal vitals
– Get a head CT if you see or suspect head trauma in the intoxicated patient
– Consider checking an alcohol level if you’re unsure. If negative, investigate further. However, remember that a positive EtOH level does not preclude other problems also being present and should not be falsely reassuring.
References / Further Reading
- Centers for Disease Control and Prevention. (2015). Early Release of Selected Estimates Based on Data. Retrieved from Centers for Disease Control and Prevention: https://www.cdc.gov/nchs/data/nhis/earlyrelease/earlyrelease201605.pdf
- Centers for Disease Control and Prevention. (2014). FastStats – Alcohol use. Retrieved from National Center for Health Statistics: https://www.cdc.gov/nchs/fastats/alcohol.htm
- Stahre M, Roeber J, Kanny D, et al. Contribution of excessive alcohol consumption to deaths and years of potential life lost in the United States. Prev Chronic Dis 2014; 11:E109.
- Hoffman, R., Howland, M., Lewin, N., Nelson, L., & Goldfrank, L. (2015). Goldfrank’s Toxicologic Emergencies, Tenth Edition. McGraw-Hill Education, 492-506, 789-90, 983-88, 1006, 1084, 1087-88, 1095-7, 1108-1112, 1346-53
- Cryer, P. (2007, April). Hypoglycemia, functional brain failure, and brain death. Journal of Clinical Investigation, 117(4): 868-70.
- Balentine J, Gaeta T, Kessler D, Bagiella E, Lee T. Effect of 50 milliliters of 50% dextrose in water administration on the blood sugar of euglycemic volunteers. Acad Emerg Med. 1998;5(7):691-694.
- Corrigan JD, Rust E, Lamb-Hart GL. The nature and extent of substance abuse problems in persons with traumatic brain injury. J Head Trauma Rehabil 1995;10(3):29-46.
- Tien, H. C., Tremblay, L. N., & Rizoli, S. B. (2006). Association Between Alcohol and Mortality in Patients With Severe Traumatic Head Injury. Archives of Surgery, 141(12), 1185-1191. Retrieved from http://jamanetwork.com/journals/jamasurgery/fullarticle/399410
- Fernandes PM, Whiteley WN, Hart SR, et al. Strokes: Mimics and chameleons. Pract Neurol 2013;13:21–28
- Annegers JF, Hauser WA, Lee JR, Rocca WA. Incidence of acute symptomatic seizures in Rochester, Minnesota, 1935-1984. Epilepsia 1995; 36:327.
- Huff JS, Morris DL, Kothari RU, et al. Emergency department management of patients with seizures: a multicenter study. Acad Emerg Med 2001; 8:622.
- Glaser CA, Honarmand S, Anderson LJ, et al. Beyond viruses: clinical profiles and etiologies associated with encephalitis. Clin Infect Dis 2006; 43:1565.
- Feigin RD, Shackelford PG. Value of repeat lumbar puncture in the differential diagnosis of meningitis. N Engl J Med 1973; 289:571.
- Misra UK, Kalita J. Neurophysiological studies in herpes simplex encephalitis. Electromyogr Clin Neurophysiol 1998; 38:177.
- Macdonald, L., Kruse, J. A., Levy, D. B., Marulendra, S., & Sweeny, P. J. (1994). Lactic acidosis and acute ethanol intoxication. The American Journal of Emergency Medicine, 12(1), 32-35. PMID 8285968.
- Irwin, Richard S.; James M. Rippe (2008). Irwin and Rippe’s intensive care medicine. Lippincott Williams & Wilkins. pp. 988–999. ISBN 978-0-7817-9153-3.
- Vilstrup, H., et al. (2014). Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver. Hepatology, 60(2), 715-735. doi:10.1002/hep.27210
- Price RW, Spudich SS, Peterson J, et al. Evolving character of chronic central nervous system HIV infection. Semin Neurol 2014; 34:7
- Dal Pan GJ, McArthur JH, Aylward E, et al. Patterns of cerebral atrophy in HIV-1-infected individuals: results of a quantitative MRI analysis. Neurology 1992; 42:2125
- McCutchan JA, Wu JW, Robertson K, et al. HIV suppression by HAART preserves cognitive function in advanced, immune-reconstituted AIDS patients. AIDS 2007; 21:1109
- Ellis, R., Langford, D., and Masliah, E. (2007). “HIV and antiretroviral therapy in the brain: neuronal injury and repair”. Nat. Rev. Neurosci. 8 (1): 33–44. PMID 17180161.
- Mckinney, A. (2009). MR Imaging Findings in 56 Patients with Wernicke Encephalopathy: Nonalcoholics May Differ from Alcoholics. Yearbook of Neurology and Neurosurgery, 2009, 79-80. doi:10.1016/s0513-5117(09)79010-6
- Liechti ME, Kunz I, Greminger P, et al. Clinical features of gamma-hydroxybutyrate and gamma-butyrolactone toxicity and concomitant drug and alcohol use. Drug Alcohol Depend 2006; 81:323.
- Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med 2013; 126:S1
- Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed, McGraw-Hill, New York 2001. P.775
- Mirrakhimov AE. Hypercalcemia of Malignancy: An Update on Pathogenesis and Management. N Am J Med Sci 2015; 7:483
- Ono Y, Ono S, Yasunaga H, et al. Clinical characteristics and outcomes of myxedema coma: Analysis of a national inpatient database in Japan. J Epidemiol 2017; 27:117.
- Mulcahy AR, Watts MR. Accidental hypothermia: An evidence-based approach. Emergency Medicine Practice EBMedicine.net 2009; 11:1. http://www.cmua.nl/content/SEHLiteratuur/SEH%20literatuurbestanden/Accidental%20Hypothermia%200109.pdf.
- Headdon WG, Wilson PM, Dalton HR. The management of accidental hypothermia. BMJ 2009; 338:b2085.
- Savage, D., & Lindenbaum, J. (1986). Anemia in Alcoholics. Medicine, 65(5), 322-338. doi:10.1097/00005792-198609000-00005
- Filippi M, Rocca MA, Ciccarelli O, et al. MRI criteria for the diagnosis of multiple sclerosis: MAGNIMS consensus guidelines. Lancet Neurol 2016; 15:292.
- European Association for Study of Liver. EASL Clinical Practice Guidelines: Wilson’s disease. J Hepatol 2012; 56:671.
- Nieman LK, Biller BM, Findling JW, et al. Treatment of Cushing’s Syndrome: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2015; 100:2807.
- Bancos I, Hahner S, Tomlinson J, Arlt W. Diagnosis and management of adrenal insufficiency. Lancet Diabetes Endocrinol 2015; 3:216.
- Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev. 2011 Apr 13;(4):CD002041. doi: 10.1002/14651858.CD002041.pub3. Review. PubMed PMID: 21491385.