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CASE REPORT Table of Contents  
Ahead of print publication
Are “Accident and emergency” Specialists prepared to tackle: Secondary hyperkalemic quadriparesis: A case report and review

1 Department of Medicine, 7 Air Force Hospital, Kanpur, Uttar Pradesh, India
2 Department of Medicine, Command Hospital Air Force, Bengaluru, Karnataka, India

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Date of Submission27-May-2022
Date of Decision06-Oct-2022
Date of Acceptance17-Oct-2022
Date of Web Publication12-Nov-2022


Areflexic periodic quadriparesis due to metabolic abnormalities, especially due to hyperkalemia, is relatively less commonly seen and discussed. The presentation is remarkable, and with high degree of suspicion in an appropriate setting, diagnosis is easy. Similarly, treatment with available options at accident and emergency is hugely satisfactory. We present and discuss a case of secondary hyperkalemic quadriparesis in a patient with end-stage renal disease. We intend to discuss pathophysiology of such condition, diagnosis, and management.

Keywords: Areflexic quadriparesis, Hyperkalemia, Periodic paralysis

How to cite this URL:
Mahapatra D, Jha VK, Bhati N, Anvesh A. Are “Accident and emergency” Specialists prepared to tackle: Secondary hyperkalemic quadriparesis: A case report and review. APIK J Int Med [Epub ahead of print] [cited 2022 Dec 4]. Available from: https://www.ajim.in/preprintarticle.asp?id=361010

  Introduction Top

Areflexic quadriparesis is a common presentation in “accident and emergency (A and E)” departments. Acute-onset areflexic quadriparesis due to Guillain–Barre syndrome (GBS) and hypokalemic periodic paralysis are widely discussed and published. Hyperkalemic quadriparesis is less well known. We present a case of secondary hyperkalemic quadriparesis in a patient with end-stage renal disease and discuss pathophysiology and management.

  Case Vignette Top

A 57-year-old male with Type 2 diabetes mellitus, diabetic end-stage renal disease on twice per week maintenance hemodialysis, chronic hepatitis C, and psoriasis, presented to the A and E of our hospital with a history of weakness of limbs and inability to bear weight of few hours' duration. He noticed this weakness after getting up from sleep in the afternoon. He had difficulty in walking and experienced buckling of the knees. He required support to go to the washroom. He also experienced weakness of both the hands and had trouble holding a mug of water. He had no sensory symptoms and no bladder or bowel involvement. He had experienced similar weakness in the past on two occasions, which were transient and improved within 1 to 2 h. On one of the previous occasions, he had missed his scheduled hemodialysis sessions for 2 weeks. On this occasion, the weakness persisted for a longer duration, and hence, he decided to report to hospital. By the time he reported to the hospital, his symptoms had improved and he was able to walk without support. Clinical examination revealed a heart rate of 52 beats/min and pulse was regular. Apart from pallor and pitting bilateral lower limb edema, the rest of systemic examination was normal. An electrocardiography (ECG) examination revealed sinus bradycardia with sinus arrhythmia and tall tenting “T” waves [Figure 1]. He was immediately given injection calcium gluconate 10% 10 ml intravenous over 10 min and glucose–insulin (GI) with 50 ml of 25% dextrose solution with 10 units of rapid-acting insulin as infusion over 30 minutes. A venous blood gas (VBG) sample drawn prior showed metabolic acidosis and potassium of 7.4 mEq/L. Simultaneously obtained blood sample report received later showed a serum potassium level of 7.56 mEq/L. Immediate hemodialysis was arranged. Dietary history taken later revealed that he had been consuming banana daily as part of ritual offering to God. He was counseled regarding dietary restrictions and discharged in a stable condition with a serum potassium of 4.5 mEq/L.

He continued with regular twice per week hemodialysis sessions and again reported after 2 months with the same complaints persisting for a period of 6 to 7 h. This time, he also experienced shortness of breath. By the time he reached the hospital, he had difficulty talking. Clinical examination revealed irregular pulse with a rate of 40/min, blood pressure of 112/62 mmHg, areflexic quadriparesis, and breath holding time of 15 s. ECG and VBG were done. ECG showed broad QRS complexes with left anterior hemiblock and right bundle branch block (RBBB) pattern, absent “P” wave, and tall “T” wave [Figure 2]. VBG potassium was 7.8 mEq/L. Laboratory report obtained subsequently revealed a serum potassium of 8.1 mEq/L. He was given injection calcium gluconate and GI infusion in A and E. Urgent hemodialysis was given with potassium-free dialysate. One hour into dialysis, his symptoms resolved. After one more session of hemodialysis during subsequent days, serum potassium normalized. ECG of this period is attached for comparison [Figure 3]. Dietary history revealed that he had consumed oranges on the insistence of his son. The need for dietary restriction was re-emphasized and he was discharged.
Figure 1: ECG showing sinus bradycardia and tall T waves. ECG: Electrocardiography

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Figure 2: ECG showing absent “P” wave, broad QRS complexes, LAHB and RBBB pattern, tall “T” wave. ECG: Electrocardiography

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Figure 3: ECG when serum potassium was normal. ECG: Electrocardiography

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  Discussion Top

Flaccid quadriparesis is a common presentation at A and E. Differential diagnosis includes traumatic spinal cord injury, botulism, GBS, drug-induced, and metabolic abnormalities.[1] GBS and hypokalemic periodic paralysis are more commonly encountered. Hyperkalemic periodic paralysis (HyPP) is less common and has less often been discussed in literature. HyPP is caused due to familial autosomal dominant muscle channelopathies.[2] This variant is called primary HyPP and is manifested at an early age. Secondary hyperkalemic flaccid quadriparesis is caused in setting of renal insufficiency, potassium sparing diuretics, potassium supplements, dietary excess, and Addison's disease.[3]

Mild hyperkalemia is often asymptomatic and is detected incidentally. Most patients with severe hyperkalemia suffer from fatal arrhythmias well before muscle paralysis, as cardiac muscle is more susceptible to high serum potassium than skeletal muscle. Occasionally, skeletal muscle paralysis predominates over cardiac muscle involvement and the reason for this is not clear. High extracellular concentration of potassium reduces the transmembrane gradient between the intracellular and the extracellular compartments preventing repolarization of the nerve and muscle membrane by reducing the efflux of potassium after depolarization. The membrane remains depolarized and refractory to any further stimulation. Nonpropagation of action potential is manifested as slowed conduction velocity and increased latencies, occasionally even conduction block, in nerve-conduction studies. Consequently, skeletal muscle contraction cannot occur, and paralysis ensues.[3],[4] Other contributory factors may include metabolic acidosis, hyponatremia, and hypoxia, all of which impair the Na+/K+ ATPase membrane pump, thereby interfering with the generation of action potential.[4]

In case of our patient, the symptoms on the first 3 occasions were transient and improved on its own. The reason for transiency of weakness while hyperkalemia was persisting is not clear. Our patient was nonoliguric and was taking frusemide diuretic, which may have partially corrected the hyperkalemia leading to resolution of symptoms.

Definitive treatment is quite rewarding and leads to rapid resolution of symptoms. Injectable calcium gluconate or calcium chloride 10% solution 10 ml as slow intravenous over 10 minutes stabilizes the myocardial membrane and effect is transient. GI infusion, sodium bicarbonate infusion, salbutamol nebulization, and frusemide diuretic intravenously will lead to permanent mitigation of serum hyperkalemia. In the setting of accompanying renal insufficiency, renal replacement therapy should be considered and will lead to quick reduction of serum potassium. Potassium-free dialysate is widely available and can be used.

High index of suspicion in the correct setting is required to pick the diagnosis. 12-lead ECG, blood gas analysis, and serum electrolyte assay can easily give away the diagnosis and should be done in all cases of flaccid quadriparesis.[4]

  Conclusion Top

Hyperkalemic quadriparesis in an appropriate setting can be diagnosed with ease when maintaining high degree of suspicion and with available amenities at any A and E. Early institution of therapy is rewarding with resolution of symptoms. Early diagnosis and therapy can often avert fatality which usually is due to cardiac effect of hyperkalemia.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given her consent for images and other clinical information to be reported in the journal. The guardian understands that her names and initials will not be published and due efforts will be made to conceal the patient's identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Muensterer OJ. Hyperkalaemic paralysis. Age Ageing 2003;32:114-5.  Back to cited text no. 1
Quiroga-Carrillo M, Correa-Arrieta C, Ortiz-Corredor F, Suarez-Obando F. Hyperkalemic periodic paralysis: Case report with a SCNA4 gene mutation and literature review. Case Rep Genet 2020;2020:8843410.  Back to cited text no. 2
Naik KR, Saroja AO, Khanpet MS. Reversible electrophysiological abnormalities in acute secondary hyperkalemic paralysis. Ann Indian Acad Neurol 2012;15:339-43.  Back to cited text no. 3
[PUBMED]  [Full text]  
Cumberbatch GL, Hampton TJ. Hyperkalaemic paralysis – A bizarre presentation of renal failure. J Accid Emerg Med 1999;16:230-2.  Back to cited text no. 4

Correspondence Address:
Debasish Mahapatra,
Department of Medicine, 7 Air Force Hospital, Nathu Singh Road, Kanpur Cantt., Kanpur - 208 004, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ajim.ajim_69_22


  [Figure 1], [Figure 2], [Figure 3]


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