A 20 Month-Old Male
It is a busy Wednesday afternoon in your pediatric emergency department. You work at a tertiary center, so you are used to receiving transfers from other hospitals for further evaluation and management. You see a new patient on the board. It is a 20 month-old male who came in as a hospital transfer for evaluation of first-time seizure. You go to bedside to start your evaluation. Parents tell you that he had three episodes of seizures in the past 6 hours. All of them lasted for less than 15 minutes, did not require medication for cessation, one of them was described as partial-focal and two were described as generalized tonic-clonic seizures, and the patient had complete return to baseline behavior a few minutes after each episode. Mom says that the patient had his axillary temperature taken by her at home and by the staff at the outside hospital and he had no fever on these measurements. However, she did notice some runny nose in the past 24 hours. As soon as the mom tells you that information, the nurse looks at you and says that the patient’s rectal temperature is 40.1 C.
The first-step in the management of febrile seizures is to understand its definitions. Following that, we need to appropriately classify the patient’s presentation within one of the two types of febrile seizure.
- Age greater than six-months-old and lower than five-years-old
- Seizure in a patient with a temperature higher than 38 C
- No inflammation or infection of the central nervous system
- No metabolic abnormality that may cause seizures
- No history of afebrile seizures
Two Types of Febrile Seizures
|Class||Age||Number of seizures in 24h||Duration||Type of seizure||Resolution||Return to baseline|
6 mo to 5 yo
< 15 min
No focal features
No meds required
6 mo to 5 yo
> 15 min
No return to baseline in a reasonable time
You must note that you will be able to easily identify those patients who fit the criteria for simple febrile seizures and those who fit the criteria for complex febrile seizures. However, there will be a group of patients that fill one or two criteria for complex febrile seizure, but are extremely well-appearing. We will talk more about that later on during the discussion.
Simple Febrile Seizures
The evaluation of a child with a simple febrile seizure should focus on the underlying febrile illness. In the vast majority of the cases the cause for the fever will be a viral infection that does not require further evaluation and treatment other than some acetaminophen (paracetamol), ibuprofen, and oral hydration.
However, as part of your job, you need to think outside of the box and have a broad differential diagnosis for your patient’s presentation. Make sure to rule out signs of CNS infection (altered mental status, nuchal rigidity, petechial rashes, and prolonged, focal or multiple seizures); risk factors, symptoms, and signs of systemic conditions that could be causing a seizure; and, history of afebrile seizures. Special factors that increase the risk for CNS infections and that you should consider in your evaluation are age 6 -12 months with incomplete immunization status (Haemophilus influenzae type b (Hib) or Streptococcus pneumoniae) and pre-treatment with antibiotics for another disorder (which could mask meningitis).
Complex Febrile Seizure in Ill-Appearing Child
The workup in this situation is simple. The patient has meningitis until proven otherwise. You should consider starting antibiotics immediately and obtaining a full sepsis workup including complete blood cell count, urinalysis, urine culture, blood cultures, chest x-ray, and lumbar puncture for cerebrospinal fluid analysis. In addition to the infectious work-up, the differential also includes epileptic seizures, toxic ingestion, metabolic disorders, head trauma, and intracranial hypertension.
Complex Febrile Seizure in Well-Appearing Child
Now we reached the tricky part of the discussion. There are no consensus guidelines for the workup of patients with complex febrile seizures in the well-appearing child. As stated in the simple febrile seizure section, you should consider further workup if any concerns for CNS infection, systemic conditions causing seizures, or history of afebrile seizures. You should decide which workup to perform on a case by case basis. In a perfect scenario, these cases should be evaluated in conjunction with specialist consultation (e.g. with pediatric neurology) for guidance with work-up and treatment.
After you finish your assessment, you make the diagnosis of complex febrile seizure because the patient had multiple seizures in less than 24 hours and had one episode with focal features. The patient is well-appearing, is fully vaccinated, has not used antibiotics recently, returns to baseline completely soon after an episode, and has no findings concerning for CNS infection on his exam. Therefore, you think that a CNS infection is less likely. Since you are facing a case of complex febrile seizure in a well-appearing child, you consult pediatric neurology for guidance with the workup and treatment. They agree with the low likelihood of CNS infection and recommend symptomatic treatment for the patient’s likely upper respiratory infection with observation during six hours in the ED. The patient has no problems during the period of observation. You re-discuss the case with pediatric neurology and they recommend discharge home with close follow-up on their clinic for further workup of other causes of seizure. A couple days later, you check the patient’s records and find that he had a spot EEG done, which was negative for epileptiform waves, and a brain MRI performed, which was unremarkable. Patient was diagnosed with complex febrile seizure and recommended to keep follow-up with his primary care physician with no need for further follow-up with pediatric neurology.
- Always obtain a temperature from a core source, in the ED the most feasible source is a rectal temperature
- The differential diagnosis for febrile seizures includes CNS infections, epileptic seizures, toxic ingestion, metabolic disorders, head trauma, and intracranial hypertension
- There is no consensus about the workup and treatment of the well-appearing patient with a complex febrile seizure
References and Further Reading
Festekjian A. Seizures and Status Epilepticus in Children. In: Cydulka RK, Fitch MT, Joing SA, Wang VJ, Cline DM, Ma O. eds. Tintinalli’s Emergency Medicine Manual, 8e New York, NY: McGraw-Hill; . http://accessemergencymedicine.mhmedical.com/content.aspx?bookid=2158§ionid=162271372. Accessed May 12, 2019.
John J Millichap. Clinical features and evaluation of febrile seizures. Mar 25, 2019. https://www.uptodate.com/contents/clinical-features-and-evaluation-of-febrile-seizures?source=history_widget
Your shift has just started, and you received a 56-year-old female patient, brought by her family due to a sudden loss of movement. The patient seems awake; you approach her, introduce yourself, and ask for her name. She does not understand. You ask her to look at you and to raise her arms, then you see: the left side of her body was paralyzed. In your head, a stroke sign lights up: you need to decide whether to activate the stroke protocol immediately or not, after all:
Time Is Brain
Neurons are very sensitive to changes in brain flow and die within minutes in the absence of perfusion: thus the urgency in attempting rapid reperfusion. (2)
Do not delay the patient evaluation because the emergency department is overcrowded! Move the patient to a monitored bed as soon as possible.
While the patient is being monitored, continue your focused neurological examination quickly and accurately. Asking for the patient to lift and hold the arms, then the legs, tests sensitivity and strength. Then you should ask her to try to smile, assess the eye movement, pupils, search for nystagmus, and ask her to try to expose the tongue, assessing movement and understanding. You ask her simple questions: full name, date, where she is, point to a cell phone, a mug and a watch and ask if she recognizes them. At the same time, you evaluate strength, orientation and deficits.
Blood Pressure: 180/110 mmHg
Pulse: 125 bpm
Respiratory Rate: 18 bpm
Do not forget to measure capillary GLUCOSE (135mg/dl). Important to rule out other causes of neurological symptoms that can mimic a stroke.
Hypoglycemia is the first condition we evaluate for when the patient presents with acute neurological deficit, decreased level of consciousness, weakness, syncope, convulsion, etc. Hypoglycemia is defined by a blood glucose level less than 45 mg/dl. Symptoms improve rapidly as soon as corrected in most cases. However, it may take time for a complete improvement, and does not always rule out a stroke. (3)
Seizure and post-ictal condition are also conditions that can mimic a stroke. Todd’s Paralysis is a focal weakness localized to one side of the body, which occurs around 13% of seizures. These deficits usually last up to 20 minutes but may last 48 hours. Unfortunately, seizures may present in the setting of acute stroke or patients with a stroke history due to neuronal damage. (3)
Stroke mimics are common, accounting for 5% to 31% of patients with acute focal neurological deficit. (3) Diagnosis is not always simple, and abnormal eye movements, increased diastolic blood pressure greater than 90mmHg, and history of atrial fibrillation or angina are most commonly found in stroke. In the presence of decreased level of consciousness, cognitive dysfunction and normal eye movements are more common in stroke mimics.
Misdiagnosed as stroke (%)
Transient global amnesia
From Konrad CN, Crocco T, Biola J, Larrabee H. Is it stroke, or something else? The Journal of Family Practice. 2010 Jan; 59 (1): 26-31.
The time is ticking, and you must make critical decisions.
Management of acute stroke will depend on:
- The support you have.
- Time of onset of the stroke, that is, duration of symptoms.
- The severity of symptoms:
- Physical examination: NIHSS, etc.
- Signs of a large vessel stroke
- Area of irreversible ischemia “core” versus penumbra area, salvageable area
- The desire of the patient/family after being informed of the risks/benefits.
The clinical history must be acquired quickly and directly. Essential points: time of symptoms, associated symptoms, comorbidities, and medications of continuous use.
It is important to note that the time of the symptom is counted from the last time the patient was seen without symptoms and not when someone noticed the deficit. (1) If the patient woke up with the deficit, time counts from when he/she was seen without symptoms (e.g., the day before bedtime).
Laboratory, Imaging, Management
Unnecessary tests should not delay brain imaging. It should be performed within 20 minutes of the patient’s arrival at the hospital!
If you do not have a CT scanner in your hospital, the patient should be referred for a center that has one, preferably with a stroke unit. In this situation, physical examination and accurate data of the clinical history must be passed to the place of reference. A physician should accompany the patient.
Treatment of blood pressure only if BP> 220 x 110mmHg, preferably with easy-to-control intravenous medication (labetalol, nicardipine, sodium nitroprusside, etc.). Avoid oral medications due to bronchospasm risk and unpredictable effect. Not having intravenous options, I would consider tolerating hypertension until the diagnosis is confirmed.
Venous access with the collection of samples such as complete blood count, electrolytes, renal function, TAP, APTT, troponin, and more as needed, according to patient comorbidities and medications.
Do not delay the brain image waiting for the collection of laboratory tests. Do not delay imaging or therapy with tPA expecting laboratory test results, unless it is essential.
Venous access before the examination is essential if there is a decision to perform CT angiography of cervical and intracranial vessels in the possibility of mechanical thrombectomy. However, performing CTA should not delay the performance of chemical thrombolysis if indicated. That is, the radiology sector should be prepared to perform immediately after CT if indicated.
Which imaging test is the best? and Why?
Weighted MRI diffusion shows a greater positivity than CT in the first 24 hours for ischemic stroke, especially in the vertebrobasilar territory. However, its role in ED is still limited because of its uncertain accuracy for the diagnosis of acute hemorrhage, low immediate availability, patient contraindications (not cooperating, claustrophobia, metal implants, pacemaker, etc.) and cost-effectiveness.
CT without contrast, is relatively accessible in most reference centers. It discards other causes of neurological deficit such as ICH, abscess, brain tumor, etc. It may not diagnose acute stroke. But together with a compatible clinical story, it is the only necessary brain image for performing IV alteplase. (2)
Every patient with acute neurological deficit, independent of time, must perform a brain imaging, mainly to rule out other causes, such as ICH, which completely changes the treatment.
All patients with acute neurological deficits, mainly without a diagnosis, must be accompanied by a physician assistant during transfer to imaging, due to the risk of abrupt change/worsening of the clinical status.
It is important to have communication between the ED areas, to warn the radiology department in advance that the patient is on the way, and that the exam should be prioritized. (2)
You accompany the patient during the CT scan. And this is her exam:
Do the best you can, ask for help when in doubt, study and care with love.
To Be Continued.
References and Further Reading
- Tintinalli, Judith E.,, et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. Eighth edition. New York: McGraw-Hill Education, 2016.
- William J. Powers et al. 2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke. AHA/ASA Guideline. 2018 Mar;49(3):e46-e110. doi: 10.1161/STR.0000000000000158. Epub 2018 Jan 24.
- Brit Long, MD, Stroke Mimics: Pearls and Pitfalls, http://www.emdocs.net/stroke-mimics-pearls-and-pitfalls/ em 07/05/2019
While his art is now highly renowned and eulogized, Vincent Willem Van Gogh spent his lifetime in considerable obscurity, fraught with numerous unprofitable endeavors, misfortunes and various illnesses leading up to his ultimate suicide at the age of 37. Years of extensive research into the possible ailments that plagued Van Gogh near the end of his life have revealed several factors that could have contributed to both his physical symptoms as well as the art style of his paintings.
Much of Van Gogh’s neuropsychiatric symptoms, most notably his episodes of seizures, began around the time of his move to the city of Arles in southern France. While the pathology of his seizures has been most famously described by Henri Gastaut (1) as a form of temporal lobe epilepsy, the cause of his disorder remains uncertain. While it is reasonable to point to his poor diet and excessive alcohol consumption as the primary factor for his symptoms, a look into Van Gogh’s substance abuse indicates the possibility of several other causes for his convulsions.
While researchers believe there to be very little evidence of digitalis use in Van Gogh’s life, the association, at the very least, provides a useful mnemonic for medical students to familiarize themselves with the vision changes related to digitalis toxicity.
Digitalis is said to purport its effects on vision through a similar mechanism. In this case, acting on Na+/K+ ATPase channels in the retina results in changes to the arrangement of rods and cones, thereby propagating the symptoms of ‘Xanthopsia’- a term used to describe a distortion in color perception with a tendency toward visualizing colored halos.
The presumption that Van Gogh was exposed to digitalis arose from the fact that, during those times, digitalis (extracted from the plant species, known commonly as the foxglove) may have been used to treat epilepsy. In fact, a plant resembling the foxglove was noted in Van Gogh’s portrait of his psychiatrist (Figure 4).
Worsening Mental State
Finally, great debate exists surrounding the cause for Van Gogh’s worsening mental state during the last years of his life. While everything from malnutrition to Acute Intermittent Porphyria has been implicated in the development of his cognitive decline, an interesting toxicological cause that may have been, at least in part, a culprit for his condition is lead poisoning.
Since most of the information obtained on Van Gogh’s illness is extracted from unreliable accounts and excerpts of letters he wrote toward the end of his life, any causal association, toxicological or otherwise, would ultimately be pure conjecture. At the very least, however, the relations outlined above provide an educational insight into the possibilities and mechanisms by which the substances prevalent in Van Gogh’s lifestyle could, in part, be contributory to his tendencies and even his psychiatric disease.
References and Further Reading
- Gastaut H: La maladie de Vincent van Gogh envisagée a la lumière des conceptions nouvelles sur l épilepsie psychomotrice. Ann Méd Psychol (Paris) 1956; 114:196–238
- Hemphill RE (1961): The illness of Vincent van Gogh. Proc Roy Soc Med 54: 1083–1088
- Simonetti G. Simon & Schuster’s Guide to Herbs and Spices. New York: Simon & Schuster; 1990. pp. 261–262
- Hold K M, Sirisoma S I, Ikeda T, Narahashi T, Casida J E. Proc Natl Acad Sci USA. Alpha-thujone (the active component of absinthe): gamma-aminobutyric acid type A receptor modulation and metabolic detoxification. 2000;97:3826–3831
- Richter CP. Self-selection of diets. Essays in Biology. Berkeley, CA: University of California Press; 1943
- Vincent van Gogh: chemicals, crises, and creativity, Author: Wilfred Niels Arnold, Published by Birkhäuser, 1992
- Phelan WJ, 3rd. Camphor poisoning: over-the-counter dangers. Pediatrics 1976; 57:428–431, Klingensmith WR. Poisoning by camphor. J Am Med Assoc 1934; 102:2182–2183
- Pande TK, Pani S, Hiran S, Rao VVB, Shah H, Vishwanathan KA (1994) Turpentine poisoning: a case report. Forensic Sci Int 65: 47–49
You are working an evening shift during your first year as an Emergency Medicine resident. A new patient shows up on the board. You briefly check his information, and you learn that he is a 32-year-old male with history of alcohol abuse coming into the Emergency Department for anxiety and tremors.
Triage note says in bold: “last drink 50 hours ago.” The patient is tachycardic, hypertensive, and mildly tachypneic.
You go to see the patient and based on the information you got, you diagnose him with alcohol withdrawal syndrome complicated by withdrawal delirium (delirium tremens). Good! You have a clinical diagnosis, but what does this patient need for workup and management?
There are two different ethanol action in the central nervous system (CNS) that lead to symptoms of alcohol withdrawal. Overall, alcohol is a central nervous system depressant. It simultaneously increases inhibitory tone via modulation of GABA activity and decreases excitatory tone via modulation of excitatory amino acid activity. In a patient with alcohol abuse disorder, only a constant presence of alcohol keeps the necessary homeostasis. Sudden cessation unmasks the adaptive responses to chronic ethanol use, resulting in overactivity of the central nervous system.
Gamma-Aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the brain. Highly specific binding sites for ethanol are found on the GABA receptor complex. Chronic ethanol use induces GABA receptor insensitivity to GABA resulting in a need for a stronger inhibitory stimulus to maintain a constant inhibitory tone. As alcohol tolerance develops, the individual retains arousal at alcohol concentrations that would normally produce lethargy or even coma in people who do not have alcohol use disorder. Sudden cessation of alcohol intake or a reduction from chronically elevated concentrations results in decreased inhibitory tone due to the lack of inhibitory effects of ethanol.
Glutamate is one of the major excitatory amino acids. When glutamate binds to the N-methyl-D-aspartate (NMDA) receptor, calcium influx leads to neuronal excitation by binding to the glycine receptor on the NMDA complex. Ethanol inhibits glutamate-induced excitation. Adaption occurs by increasing the number of glutamate receptors in an attempt to maintain a normal state of arousal.
Alcohol withdrawal remains a clinical diagnosis. The severity of presentation can be assessed using a clinical assessment scale called Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar) that can be found on MD Calc.
In some cases, several additional tests might be needed to rule out other conditions that mimic or coexist with alcohol withdrawal syndrome. This is especially true when the patient has altered mental status and fever. Conditions such as infection (e.g., meningitis), trauma (e.g., intracranial hemorrhage), metabolic abnormalities, drug overdose, hepatic failure, and gastrointestinal bleeding can mimic or coexist with alcohol withdrawal. Also, it is of marked importance to try to understand why the patient stopped consuming alcohol. If you establish that he wanted to get sober, that is great, you or the admitting team can help setting up rehab for him after the acute problems are controlled. However, you should get suspicious if there is not a clear cause for the abrupt cessation of alcohol intake since it could be an acute condition being masked by the withdrawal syndrome.
Initial workup might include:
As important as proving control of the patient’s withdrawal symptoms is to provide high-quality supportive care, which includes:
The basis for the treatment of alcohol withdrawal is CNS depressants, such as benzodiazepines, with a treatment goal of Richmond Agitation and Sedation Scale (RASS) -1 and HR < 110. No single drug benzodiazepine is superior to another. A common treatment strategy is to use a benzodiazepine of choice and give escalating doses until symptomatic control or until you reach criteria for refractory alcohol withdrawal.
Refractory Withdrawal Delirium
Some patients have refractory delirium tremens (DT) despite treatment with high-dose benzodiazepines. Refractory DT is not clearly defined. It may be present if symptoms of severe withdrawal are not controlled adequately after the IV administration of more than 50 mg of diazepam or 10 mg of lorazepam during the first hour of treatment, or 200 mg of diazepam or 40 mg of lorazepam during the initial three to four hours of treatment. In such cases, as with any dangerous toxicologic disorder, you should obtain assistance from a medical toxicologist or poison control center. In case you diagnose your patient with alcohol withdrawal refractory to benzodiazepine treatment, you should have a few other options in your treatment arsenal.
There are case reports of up to 2000 mg of Phenobarbital administered orally or intravenously on the first day in patients with alcohol withdrawal delirium. Consider giving phenobarbital 130 to 260 mg IV, repeated every 15 to 20 minutes, until symptoms are controlled. Also, you can consider administering Phenobarbital earlier in the disease course. A randomized trial of 102 patients presenting to the emergency department with acute alcohol withdrawal, those treated with lorazepam and a single dose of Phenobarbital had substantially lower ICU admission rates compared with those treated with lorazepam alone (8 versus 25 percent).
Another adjunctive medication for alcohol withdrawal is dexmedetomidine, an α2-adrenergic agonist that is used to provoke a state in which the patient is sedated but arousable, with a decreased sympathetic tone. Doses up to 0.7 μg per kilogram per hour have been administered in patients who do not have a good response to benzodiazepines. Heart block is a contraindication to this drug since it can cause bradycardia. In case it is given, blood pressure and heart rate must be closely monitored.
Propofol and Intubation
In patients who do not have a response to high doses of benzodiazepines (especially patients who are intubated), propofol may be administered to reach symptomatic control.
- Schuckit, MA. “Recognition and Management of Withdrawal Delirium (Delirium Tremens)”, N Engl J Med 2014; 371:2109-2113
- Hoffman, RS and Weinhouse, GL. “Management of moderate and severe alcohol withdrawal syndromes”, UpToDate, Dec 18, 2018. Available at https://www.uptodate.com/contents/management-of-moderate-and-severe-alcohol-withdrawal-syndromes
- Weingart, S. “EMCrit Podcast 11 – Delirium Tremens”, EMCrit RACC, Sep 29, 2009. Available at https://emcrit.org/emcrit/delirium-tremens/
- Isbell H, Fraser HF, Wilker A, et al. An experimental study of the etiology of rum fits and delirium tremens. Q J Stud Alcohol 1955; 16:1.
- Mihic SJ, Ye Q, Wick MJ, et al. Sites of alcohol and volatile anaesthetic action on GABA(A) and glycine receptors. Nature 1997; 389:385.
- Morrow AL, Suzdak PD, Karanian JW, Paul SM. Chronic ethanol administration alters gamma-aminobutyric acid, pentobarbital and ethanol-mediated 36Cl- uptake in cerebral cortical synaptoneurosomes. J Pharmacol Exp Ther 1988; 246:158.
- Hoffman PL, Grant KA, Snell LD, et al. NMDA receptors: role in ethanol withdrawal seizures. Ann N Y Acad Sci 1992; 654:52.
- Hecksel KA, Bostwick JM, Jaeger TM, Cha SS. Inappropriate use of symptom-triggered therapy for alcohol withdrawal in the general hospital. Mayo Clin Proc 2008; 83:274.
- Hack JB, Hoffman RS. Thiamine before glucose to prevent Wernicke encephalopathy: examining the conventional wisdom. JAMA 1998; 279:583.
- Hoffman RS, Goldfrank LR. The poisoned patient with altered consciousness. Controversies in the use of a ‘coma cocktail’. JAMA 1995; 274:562.
- Hoffman RS, Goldfrank LR. Ethanol-associated metabolic disorders. Emerg Med Clin North Am 1989; 7:943.
- Mainerova B, Prasko J, Latalova K, et al. Alcohol withdrawal delirium — diagnosis, course and treatment. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 2013;157:1-9
- Mayo-Smith MF, Beecher LH, Fischer TL, et al. Management of alcohol withdrawal delirium: an evidence-based practice guideline. Arch Intern Med 2004;164:1405-1412
- Amato L, Minozzi S, Vecchi S, Davoli M. Benzodiazepines for alcohol withdrawal. Cochrane Database Syst Rev2010;3:CD005063-CD005063
- Hjermø I, Anderson JE, Fink-Jensen A, Allerup P, Ulrichsen J. Phenobarbital versus diazepam for delirium tremens — a retrospective study. Dan Med Bull 2010;57:A4169-A4169
- DeCarolis DD, Rice KL, Ho L, Willenbring ML, Cassaro S. Symptom-driven lorazepam protocol for treatment of severe alcohol withdrawal delirium in the intensive care unit. Pharmacotherapy 2007;27:510-518
- DeBellis R, Smith BS, Choi S, Malloy M. Management of delirium tremens. J Intensive Care Med 2005;20:164-173
- Cagetti E, Liang J, Spigelman I, Olsen RW. Withdrawal from chronic intermittent ethanol treatment changes subunit composition, reduces synaptic function, and decreases behavioral responses to positive allosteric modulators of GABAA receptors. Mol Pharmacol 2003; 63:53.
- Nolop KB, Natow A. Unprecedented sedative requirements during delirium tremens. Crit Care Med 1985; 13:246.
- Hack JB, Hoffmann RS, Nelson LS. Resistant alcohol withdrawal: does an unexpectedly large sedative requirement identify these patients early? J Med Toxicol 2006; 2:55.
- Rosenson J, Clements C, Simon B, et al. Phenobarbital for acute alcohol withdrawal: a prospective randomized double-blind placebo-controlled study. J Emerg Med 2013; 44:592.
- Rayner SG, Weinert CR, Peng H, Jepsen S, Broccard AF. Dexmedetomidine as adjunct treatment for severe alcohol withdrawal in the ICU. Ann Intensive Care 2012;2:12-12
- Muzyk AJ, Fowler JA, Norwood DK, Chilipko A. Role of α2-agonists in the treatment of acute alcohol withdrawal. Ann Pharmacother 2011;45:649-657
- Thomson AD, Cook CCH, Touquet R, Henry JA. The Royal College of Physicians report on alcohol: guidelines for managing Wernicke’s encephalopathy in the accident and emergency department. Alcohol Alcohol 2002;37:513-521
- Koethe D, Juelicher A, Nolden BM, et al. Oxcarbazepine — efficacy and tolerability during treatment of alcohol withdrawal: a double-blind, randomized, placebo-controlled multicenter pilot study. Alcohol Clin Exp Res 2007;31:1188-1194
by Stacey Chamberlain
A 24-year-old woman presents with headache that began three hours prior to arrival to the ED. The patient was at rest when the headache began. The headache was not described as “thunderclap,” but it did reach maximum severity within the first 30 minutes. The headache is generalized and rated 10/10. She denies head trauma, weakness, numbness, and tingling in her extremities. She denies visual changes, changes in speech and neck pain. She has not taken anything for the headache. She does not have a family history of cerebral aneurysms or polycystic kidney disease. On physical exam, she has a normal neurologic exam and normal neck flexion.
Should you do a head CT and/or a lumbar puncture to evaluate for a sub-arachnoid hemorrhage in this patient?
Ottawa SAH Rule
Investigate if ≥1 high-risk variables present
- Age ≥ 40
- Neck pain or stiffness
- Witnessed loss of consciousness
- Onset during exertion
- Thunderclap headache (instantly peaking pain)
- Limited neck flexion on exam
A CDR to determine risk for sub-arachnoid hemorrhage (SAH) was derived and has been externally validated in a single study. The CDR’s purpose was to identify those at high risk for SAH and included those with acute non-traumatic headaches that reached maximal intensity within one hour and who had normal neurologic exams. Of note, the rule has many inclusion and exclusion criteria that the ED physician must be familiar with and was only derived for patients 16 years or older. The study authors note that the CDR is to identify patients with SAH; it is not an acute headache rule. In the validation study, of over 5,000 ED visits with acute headache, only 9% of those met inclusion criteria. Also, clinical gestalt again plays a role as the authors suggest not to apply the CDR to those who are ultra-high risk with a pre-test probability for SAH of > 50%.
The Ottawa SAH Rule was 100% sensitive but did not lead to reduction of testing vs. current practice. The authors state that the value of the Ottawa SAH Rule would be to standardize physician practice in order to avoid the relatively high rate of missed sub-arachnoid hemorrhages.
By applying the Ottawa SAH Rule, this patient is low risk and does not require further investigation for a SAH.
A young man presented after a new onset seizure.
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In case you didn’t encounter acute altered mental status and right side weakness today!