Case Presentation by Dr. Jamie Kenney-Kalbuneh
HISTORY OF PRESENT ILLNESS
47 year old male presented to the emergency department with the chief complaint of weakness. Over the past two days he had progressively worsening weakness of his upper and lower extremities. Two days prior his legs felt weak and he was unsteady when walking around the house. It became gradually worse over the next 24 hours to the point he was unable to get out of bed. The evening prior to arrival in the ED he noticed his arms became weak and he was unable to dress himself the next morning. He also noticed that it was becoming hard for him to hold his head up and he began experiencing a tingling sensation in his hands and feet. Patient had missed his last dialysis session due to having a recently clotted A-V Fistula. He last received dialysis four days prior with no complications.
The patient denied shortness of breath, chest pain, cough, weight loss, nausea or vomiting. No symptoms of fecal or urinary incontinence. Denied any history of fever or chills, denied any sick contacts or recent travel. No history of trauma. Denied any new medication or changes to the dosing of his medication.
PMHx: HTN, SLE and ESRD secondary to lupus nephritis
SOCIAL: Tobacco use, ½ ppd x 20years, negative for alcohol or drug use.
MEDICATIONS: Metroprolol, Amlodipine, Phoslo, Vitamin D, acetaminophen with hydrocodone
Constitutional: Well developed middle age male in no acute distress. He was resting comfortably on the stretcher and speaking in complete sentences.
Vital signs: BP 221/111 HR 71 RR 18 Temp 35.1 and Pulse ox 98% on room air.
Skin: Warm and dry, normal capillary refill. Radial and dorsalis pedis pulses were 2+ and equal bilaterally.
HEENT: Normal cephalic, no signs of trauma. Pupils 3mm and equal, EOMI. No visual field deficits. Moist mucus membranes, no intraoral lesions or thrush
Neck: Trachea midline, no JVD. When patient was asked to turn his head toward one shoulder or lift his head off the bed he was unable. When his head was passively lifted off the stretcher it would fall back down. No neck pain, neck was supple.
Lungs: CTABL with normal respiratory effort
CV: S1/S2 regular rate and rhythm
Abdomen: Soft, non-tender to palpation, normal bowel sounds.
Rectal: Guaiac negative stool, normal rectal tone and a normal sized, non-tender prostate.
Musculoskeletal: No edema, no atrophy
Neurological: Patient was awake, alert and oriented. No facial asymmetry or dysarthria. No nystagmus or clonus. Follows commands appropriately. No tounge deviation. Strength in bilateral lower extremities was 0/5, 1/5 in the upper extremities and 3/5 in the hands bilaterally. Sensation was decreased to light touch in all four extremities. Grade 0 reflexes in bilateral biceps, triceps, patella and ankle. Downgoing plantar reflex. Unable to asses gait or perform cerebellar testing secondary to weakness.
Ca 9.8 Mg 2.9
INR 0.9 PT 10.2 PTT 39.3
Question #1 Based on your interpretation of the EKG was should you do next?
A) Place pacer pads on patient in preparation for cardioversion
B) Give calcium gluconate
C) Amiodarone 150mg bolus followed by a drip
D) Activate STEMI pager
Question #2 What other testing should be performed in this patient?
A) Stat ECHO
B) Stat EEG
C) Lumbar puncture
D) CTA-Head and Neck
Question #3 What immediate intervention needs to be done?
A) To the OR for aortic dissection repair
B) Begin treatment with high-dose IVIG
C) Broad spectrum antiobiotic therapy with Vancomyin, Cefepime and Acyclovir
D) Emergent Dialysis
Answers & Discussion
This patient presented with a typical presentation for an uncommon disease, Hyperkalemic Paralysis. Hyperkalemia is a well documented complication in ESRD patients. They commonly present with cardiac manifestations such as arrhythmias because the cardiac tissue is very sensitive to changes in potassium. However some patients with severe hyperkalemia have symptoms of muscular paralysis without any cardiac features or EKG changes. Hyperkalemia has been shown to result in abnormalities of the membrane potential of excitable tissue. At the cellular level, elevated levels of potassium reduce the transmembrane gradient between intracellular and extracellular compartments leading to partial neuronal depolarization. The degree of depolarization is directly related the degree of hyperkalemia. As a result, voltage gated sodium channels are inactivated and these partially depolarized neurons are refractory to excitation leading to muscle weakness.
Question #1 B)
This patients EKG was concerning for hyperkalemia. He has evidence of peaked T waves, prolonged PR interval with flattened P waves, widened QRS. You should immediately begin treatment for hyperkalemia, the most important of which is calcium gluconate for cardiac membrane stabilization. Treatment should also consist of sodium bicarbonate, insulin, glucose, high dose albuterol and kayexalate.
Question #2 C)
Hyperkalemic paralysis closely mimics Guillan Barré Syndrome; patients present with a rapidly ascending symmetrical paralysis. Sustained hyperkalemia is thought to exert its effect by impairing the generation of action potentials and increasing the latency of conduction. Within a few hours of symptom onset the majority of patients are no longer able to walk. General consensus recommends a lumbar puncture be performed to rule out Guillan Barré. These two conditions are often unable to be differentiated clinically. The current recommendation is to perform the lumbar puncture while at the same time treating the patients hyperkalemia.
Question #3 D)
Emergent dialysis is essential for these patients. Once patients are given treatment for hyperkalemia they should begin to have resolution of their symptoms and after the potassium level is normalized symptoms should completely resolve. Nerve excitability in patients with chronic renal failure prior to dialysis has shown there are significant abnormalities in axonal excitability in those patients with hyperkalemia. Axons were depolarized in CRF patients with elevated levels of potassium leading to reduced action potentials and a markedly prolonged relative refractory period. These abnormalities were significantly and rapidly reduced once serum potassium levels were normalized after dialysis.
Acute ascending paralysis is a rare complication of hyperkalemia but one that is potentially lethal. There have been many conditions associated with hyperkalemic paralysis including Addison’s disease, potassium sparing medications such as TMP-SMX and spironolactone and of course renal failure. My patient refused to have a lumbar puncture performed. We arranged for him to have emergent dialysis and within 30 minutes of completing dialysis he was up walking around the room asking to go home. Physicians should have a low threshold for admitting patients with hyperkalemia associated paralysis to an ICU bed as respiratory involvement rapidly leads to respiratory failure. One must also keep in mind that the use of succinylcholine for rapid-sequence intubation can be fatal to these patients secondary to cardiac arrhythmias.
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