Sensation to light touch intact in bilateral upper and lower extremities
2+ patellar reflexes bilaterally
Unable to ambulate due to weakness
Ddx for Generalized Weakness:
Hypokalemia/hyperkalemia vs rhabdomyolysis vs periodic paralysis vs spinal cord compression vs Guillain-Barre syndrome
Initial Diagnostics:
Initial labs notable for K 1.9, Mg 1.5, and Phos 1.1
Initial ECG (see below)
Management:
Electrolytes repleted as follows…
40 mEq oral K, 20 mEq IV K
2 gm Mg over 2 hours
2 tablets of Neutra-Phos
Case Progression:
Ultimately diagnosed with hyperthyroidism, likely secondary to Graves’ disease
TSH <0.01
Ultrasound thyroid
Enlarged heterogeneous thyroid with diffusely increased vascularity
Thyroid nodule of the isthmus
Started on Methimazole and Propranolol
Presenting symptoms and electrolyte abnormalities attributed to thyrotoxic periodic paralysis
Thyrotoxic Periodic Paralysis (TPP)
Potentially life-threatening
Defined as the triad of
Muscle paralysis
Acute hypokalemia
Hyperthyroidism
Less than half of TPP patients exhibit clinical signs of hyperthyroidism
Rapid recognition and termination are mandatory to avoid potentially fatal complications of severe hypokalemia
Cardiac arrhythmias
Respiratory failure
Management complicated by the thin line between refractory hypokalemia and rebound hyperkalemia
KCl supplementation is essential but often not enough to control TPP
IV propranolol has been reported to reverse weakness and hypokalemia in patients unresponsive to KCl administration
References:
Bilha S, Mitu O, Teodoriu L, Haba C, Preda C. Thyrotoxic Periodic Paralysis-A Misleading Challenge in the Emergency Department. Diagnostics (Basel). 2020;10(5):316. Published 2020 May 18. doi:10.3390/diagnostics10050316
Lin SH, Huang CL. Mechanism of thyrotoxic periodic paralysis. J Am Soc Nephrol. 2012;23(6):985-988. doi:10.1681/ASN.2012010046
A 70 year old male with a past medical history of hypertension, type 2 diabetes, and atrial fibrillation on warfarin presents for visual changes. He is accompanied by his daughter who states that about one hour ago, his vision on the right side became blurry. There is associated right facial numbness and headache. His daughter believes that he has become more confused over this time period. Fingerstick glucose is 220. An EKG is obtained which shows atrial fibrillation at a rate of 92.
Exam
BP 151/75, HR 92, T 97.8F, RR 18, SpO2 98%
Comfortable appearing in no acute distress. GCS E4 V4 M6. No facial droop. Decreased sensation to right side of face. 5/5 strength and sensation in all extremities. No difficulty with rapid alternating movements. Extraocular motion intact. Left gaze preference with right sided homonymous hemianopia.
Case continued: Neurology is emergently consulted and a stroke alert is activated. CT/CTA of the head and neck shows no acute intracranial hemorrhage and no large vessel occlusion. Labs are notable for an INR of 1.6. The decision is made in conjunction with neurology to administer thrombolytics, and the patient is admitted to neurology critical care. Repeat head CT 24 hours later demonstrates a left parieto-occiptal infarct.
Pearls:
– This patient’s neurologic deficits including right sided facial numbness, right homonymous hemianopsia, left sided gaze preference, and aphasia localize to a cortical distribution as noted above.
– Warfarin use alone is not a contraindication to thrombolytics for acute ischemic stroke. The INR must be > 1.7 in addition to be an exclusion criterion.
– This patient had multiple previous subtherapeutic outpatient INR levels which likely precipitated an embolic stroke.
– In patients without contraindications, the decision to administer thrombolytics for acute ischemic stroke should be clinical without waiting for results of laboratory testing with the exception of a point of care glucose and patients with suspected coagulopathy.
– Other common exclusion criteria to use of thrombolytics in acute ischemic stroke include previous head trauma or stroke within 3 months, any previous intracranial hemorrhage, SBP > 185 or DBP > 110, or known intracranial mass such as neoplasm or aneurysm.
References:
Go S, Kornegay J. Stroke Syndromes. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e.
Powers WJ, Rabinstein AA, Ackerson T, et al. 2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association [published correction appears in Stroke. 2018 Mar;49(3):e138] [published correction appears in Stroke. 2018 Apr 18;:]. Stroke.
HPI: A 29 year old male with a past medical history of polysubstance use presents to the ED in December via EMS for a suspected overdose. History is limited due to patient cooperation. EMS states that he was found outside in a puddle, minimally responsive. He was given 2mg IM naloxone by EMS and became acutely agitated and combative afterward, requiring 5mg IM midazolam and 5mg IM haloperidol upon arrival. Fingerstick glucose 226. ECG is obtained and shown below.
Exam: BP 182/84, HR 111, T 86.1F, RR 18, SpO2 100%
Disheveled appearing male in wet clothes, intermittently thrashing. Cold to touch. Pupils 5mm bilaterally. No signs of trauma. GCS E3 V2 M5. Moves all extremities equally. Heart rate is tachycardic and irregular
ECG interpretation: atrial fibrillation with Osborne waves
Differential diagnosis: polysubstance use, environmental cold exposure, severe sepsis, hypothyroidism
Case continued: Active rewarming is initiated by removing wet clothes, administering warmed IV fluids, and placing a bair hugger. Labs are notable for a creatinine kinase of 3966. The patient’s temperature, heart rate, and mental status significantly improve within 5 hours, and his repeat EKG shows normal sinus rhythm without Osborn waves. He is ultimately admitted to medicine.
Pearls:
– The cardiovascular response to cold is peripheral vasoconstriction and initial increase in heart rate and blood pressure. As core temperature drops below 32C, there is myocardial irritability and risk of cardiovascular collapse.
o Atrial fibrillation and flutter are common arrhythmias associated with hypothermia.
o Rescue collapse is a term to describe cardiac arrest that occurs during extrication or transport of a profoundly hypothermic patient due to profound myocardial irritability.
– Osborn waves are positive deflections at the end of the QRS complex that are non-specific but may occur in temperatures below 32C.
o Size of the wave correlates with the degree of hypothermia but has no prognostic value.
– As temperature continues to drop, EKG changes are variable but classically include bradycardia with prolonged PR, QRS, and QTc. Heart block or ventricular dysrhythmias may be encountered as well. Asystole is the common final dysrhythmia.
– Rewarming is the treatment of choice.
o Atrial dysrhythmias such as atrial fibrillation will often resolve with warming.
o Cardioversion for unstable arrhythmias should be attempted but may be refractory in severe hypothermia.
References:
Brown DA. Hypothermia. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill Education; 2020.
Hoek T. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010. 122:5829-5861
22 yo male hx of prior GSW to L chest with retained bullet presents with chief complaint of 2 days of left sided chest and left upper quadrant abdominal pain, along with intermittent nonbilious emesis
No fevers, no dyspnea, normal bowel movements
Physical Exam
VS: T 97.3 HR 80 BP 153/70 O2 98% on RA
Well appearing, in no distress
Lungs clear bilaterally, heart sounds normal
Abdomen soft, +tenderness in LUQ without guarding and rebound tenderness
No lower extremity edema
ECG:
Chest film:
Interpretation: Apparent left sided pleural effusion, not apparent on lateral view
CT chest:
Highlighted area indicates diaphragmatic hernia with portion of the stomach in the left chest
Clinical Course
NGT placed to decompress stomach
Admitted to CT surgery
Had EGD to assess viability of gastric mucosa which was normal
Underwent open surgical repair of diphragmatic hernia with reduction of stomach into abdominal cavity
Pearls
Diaphragmatic hernia is a rare condition usually a sequelae of trauma
Conventional imaging such as CT will likely not detect an acute injury to the diphragm
Patients often present late after acute trauma when visceral contents herniate into the chest cavity
Exam may demonstrate acute respiratory distress and bowel sounds on pulmonary auscultation
Patients may be in frank shock from gastric/intestinal ischemia
A 53-year-old male with a history of chronic daily alcohol use presents to the ED via EMS after a witnessed seizure at home
The medics say he drinks every day, but his last drink was 3 days ago because he was not able to go to the store (history obtained from the sister who witnessed the seizure)
Physical Examination
T 98.3F, BP 177/106, HR 191, RR 22, Sat 93%
Patient appears anxious, uncomfortable, and is actively vomiting blood tinged sputum
He appears confused and is not answering questions appropriately
He is tachycardic and his lungs are clear to auscultation bilaterally
Abd: soft NTND
Differential
Alcohol withdrawal/ Delirium Tremens
Thyrotoxicosis
Sepsis
Pulmonary embolism
Heart failure
Workup and Management
The nurse informs you that the patient is seizing
This patient is exhibiting evidence of delirium tremens (psychomotor agitation and autonomic instability) and alcohol withdrawal seizure
The patient is no longer tolerating his secretions, he is confused, gurgling, and requires a definitive airway
After intubation, you bolus the patient with propofol and start him a propofol infusion
The patient is admitted to the ICU for further management
Teaching Points
ETOH withdrawal begins 6-8 hours after last intake and peaks in 72 hours
Symptom based treatment via the CIWA score can help stratify patients, scores >15 indicate severe withdrawal
Start with IV diazepam at 10mg or lorazepam at 4mg and repeat them in doubling doses
Consider adding phenobarbital for refractory cases (i.e. after 200 mg of diazepam)
Consider propofol as the induction agent and sedative post-intubation as propofol potentiates GABA receptor activity and inhibits NMDA receptors Summary
Delerium tremens can result in death from hyperthermia, arrhythmia and seizures
Sources:
Long D, Long B, Koyfman A. The emergency medicine management of severe alcohol withdrawal. The American Journal of Emergency Medicine. 2017;35(7):1005-1011. doi:10.1016/j.ajem.2017.02.002
Schuckit MA, Author Affiliations From the Department of Psychiatry. Recognition and Management of Withdrawal Delirium (Delirium Tremens): NEJM. New England Journal of Medicine. https://www.nejm.org/doi/10.1056/NEJMra1407298. Published February 5, 2015. Accessed December 9, 2020.
Case: A 29 year old male with a past medical history of polysubstance use presents to the ED in December via EMS for a suspected overdose. History is limited due to patient cooperation. EMS states that he was found outside in a puddle, minimally responsive. He was given 2mg IM naloxone by EMS and became acutely agitated and combative afterward, requiring 5mg IM midazolam and 5mg IM haloperidol upon arrival. Fingerstick glucose 226. EKG is obtained and shown below.
Exam: BP 182/84, HR 111, T 86.1F, RR 18, SpO2 100% Disheveled appearing male in wet clothes, intermittently thrashing. Cold to touch. Pupils 5mm bilaterally. No signs of trauma. GCS E3 V2 M5. Moves all extremities equally. Heart rate is tachycardic and irregular.
EKG interpretation: atrial fibrillation with rapid ventricular response with Osborn waves
Differential diagnosis: polysubstance use, environmental cold exposure, severe sepsis, hypothyroidism
Case continued: Active rewarming is initiated by removing wet clothes, administering warmed IV fluids, and placing a bair hugger. Labs are notable for a creatinine kinase of 3966. The patient’s temperature, heart rate, and mental status significantly improve within 5 hours, and his repeat EKG shows normal sinus rhythm without Osborn waves. He is ultimately admitted to medicine.
Pearls:
The cardiovascular response to cold is peripheral vasoconstriction and initial increase in heart rate and blood pressure. As core temperature drops below 32C, there is myocardial irritability and risk of cardiovascular collapse.
Atrial fibrillation and flutterare common arrhythmias associated with hypothermia.
Rescue collapse is a term to describe cardiac arrest that occurs during extrication or transport of a profoundly hypothermic patient due to profound myocardial irritability.
Osborn waves are positive deflections at the end of the QRS complex that are non-specific but may occur in temperatures below 32C.
Size of the wave correlates with the degree of hypothermia but has no prognostic value.
As temperature continues to drop, EKG changes are variable but classically include bradycardia with prolonged PR, QRS, and QTc. Heart block or ventricular dysrhythmias may be encountered as well. Asystole is the common final dysrhythmia.
Rewarming is the treatment of choice.
Atrial dysrhythmias such as atrial fibrillation will often resolve with warming.
Cardioversion for unstable arrhythmias should be attempted but may be refractory in severe hypothermia.
References:
Brown DA. Hypothermia. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill Education; 2020.
Hoek T. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010. 122:5829-5861
A 60 year old male with a PMH of DM, HTN, HLD, MI presents to the ED after being found down with waxing and waning mentation. The patient complains of abdominal pain and diffuse myalgias.
BP 76/56, HR 92, Temp 98.4F, RR 22.
Physical exam
Pressure wounds of the right rib cage, right side of his forehead
Right calf tenderness with a firm anterior compartment, cool/pale right lower extremity, dorsalis pedis and posterior tibial pulses were unable to be palpated.
ECG:
ECG interpretation: Peaked T waves, widened QRS concerning for hyperkalemia
Clinical course:
1L bolus of LR
IV calcium gluconate for possible hyperkalemia
Surgery was immediately consulted due to concern for compartment syndrome
Labs were notable for a potassium of 7.2, creatinine of 3.49, creatinine kinase of 188,760, a lactate of 4.0, and ALT/AST in the 3,000s/5,000s
Given intermittent hemodynamic instability a dialysis line was placed for definitive hyperkalemia management
Patient underwent emergent lower extremity fasciotomy with surgery
Compartment syndrome learning points:
· Diagnosis is both clinical and by compartment pressure measurements
· Compartment pressure >30mmHg or a delta pressure <30mmHg (diastolic BP – compartment pressure) is diagnostic
· Clinical findings: 6Ps. Pain is the earliest and often only symptom, the rest are late findings.
o Pain out of proportion to the exam (most common finding)
o Pallor
o Paresthesia
o Paresis/paralysis
o Pulselessness
o Poikilothermia
· Management: Immediate surgical consult for fasciotomy
Today’s case from the EM Daily archives involves one of the rare patients where you DO want to acutely treat elevated blood pressure with intravenous agents….
HPI
48 year old male with PMH HTN presents with blurry vision for 2.5 hours
Patient was using the computer tonight, could not see where the icons were on his desktop, could still see light/colors.
He has no pain in his eyes
Also reports dyspnea on exertion for 2 days. No headache, no chest pain, no abdominal pain
He has not had his anti-hypertensives (he reports he is on 5 different medications) for about 1.5 weeks
Physical Exam
T 98.3 BP 290/120, HR 118, RR 18, SpO2 99%
Patient is awake, alert, conversant, appears well and in no distress
Neuro: Visual acuity 20/200 OS, OD, OU Normal visual fields Normal pupillary exam Normal extraocular movements Otherwise normal cranial nerve exam Normal strenght in extremities , no pronator drift, normal finger to nose
Cardiac: tachycardic, normal S1/S1, no murmurs/rubs/gallops
Pulm: clear to auscultation bilaterally
Abdomen: soft, nontender, nondistended
Differential Diagnosis
Hypertensive emergency with elevated BP and evidence of end organ damage (decreased visual acuity, evidence of pulmonary edema on bedside US)
Sympathomimetic toxicity (hypertension, tachycardia), though patient reports no ingestions of medications or drugs
Thyrotoxicosis
CVA given visual changes, however with no focal visual deficits (no visual field cut, decreased acuity is symmetric bilaterally)
Initial ED Management
Arterial line place – IV nicardipine started, with goal SBP 210s (25% reduction in the first hour)
Bedside lung US performed which demonstrates numerous B lines consistent with evolving pulmonary edema
Labs/Imaging –
Hb 6.1, PLT 142, WBC 5.92 – Na 147, K 3.7 – Cr 15.03 (last level in chart 3.95 7 years ago) – HS troponin 223 – pro-BNP 26,930
CT Head with 3 small, distinct areas of intraparenchymal hemorrhage
Further Management
Repeat neurologic exam performed and is unchanged
Neurosurgery consulted, recommend BP goal under SBP 160
Repeat CTH in 4 hours: unchanged
Patient admitted to ICU for IV nicardipine, continuous BP monitoring, and q1 hour neuro checks
Pearls
Hypertensive emergency is acute SBP over 180 with evidence of organ dysfunction
Not every patient with SBP over 180 requires emergency BP control
In this patient: decreased visual acuity, pulmonary edema, elevated troponin and proBNP, renal failure, and intraparenchymal hemorrhage = hypertensive emergency
In managing hypertensive emergency, SBP should not be lowered by more than 25% in the first hour to prevent causing hypoperfusion and cerebral ischemia
Continuous BP monitoring via arterial line is important to carefully titrate medications
Nicardepene is an easy to titrate CCB which may be the ideal agent for the treatment of hypertensive emergency
Indications for emergent dialysis (AEIOU – acidosis, electrolytes, intoxication, overload, uremia): critical metabolic acidosis, refractory or rapidly increasing hyperkalemia, life threatening intoxication with substance that is able to be removed with HD, volume overload, complications of uremia (pericarditis, neuropathy, encephalopathy)
