Acute flaccid paralysis due to multifactorial hyperkalaemia

Case presentation

A male patient in his late 30s presents to the emergency department (ED) complaining of progressive limb weakness. The patient mentioned acute lower limb weakness starting the night before admission and reduced urinary output for the last couple of days. In the morning, he noticed worsening symptoms with weakness involving all limbs and an inability to walk or lift heavy objects. The patient’s condition continued to decline throughout the day until complete paresis and no urination for 16 plus hours in the late afternoon. At admission to the ED, the patient maintained complaints with a physical examination showing symmetrical flaccid paresis with general areflexia involving all four limbs. There was no pain, numbness or sensitivity changes. Respiratory and neck muscles were also not involved. No other changes were noted.

Medical history was relevant for proctocolectomy 20 years prior due to colorectal cancer and a diagnosis of Lynch syndrome. The month prior to the ED visit, the patient was diagnosed with colorectal cancer relapse (mass measuring 76×72×112 mm with anal sphincter and pelvic muscles invasion (figure 1)), having started chemotherapy 3 days before the ED admission with surgery scheduled for the following weeks.

Figure 1

MRI showing axial T2 weighted image with pelvic mass measuring 76×72×112 mm with anal sphincter and pelvic muscle invasion, namely obturator internus and levator ani.

Investigations

The investigation was started in the emergency room with an immediate collection of arterial blood gases that showed metabolic acidosis (pH of 7.31, bicarbonate of 11.4 mmol/L, pCO2 23 mm Hg) with severe hyperkalaemia of 9.0 mmol/L and hyponatraemia of 120 mmol/L. ECG showed sinus rhythm with increased PR interval and peaked T waves (figure 2), changes that are compatible with hyperkalaemia. Blood work confirmed hyperkalaemia with potassium (K⁺) at 9.9 mmol/L, and in addition showed acute kidney injury (AKIN stage 3, with creatinine at 12.9 mg/dL and blood urea nitrogen at 152.3 mg/dL), a significant increase in uric acid (19.5 mg/dL) with a mild increase of lactate dehydrogenase (LDH). Abdominal ultrasound showed bilateral hydronephrosis with obstruction from a pelvic mass being the probable cause.

Figure 2

12 lead ECG showing sinus rhythm with an increased PR interval of 224 mg and peaked T waves.

Differential diagnosis

The differential diagnosis of acute symmetrical areflexic paresis is vast and can be roughly divided into four categories:

• Myelopathies, such as compressive lesions, transverse myelitis and poliomyelitis.

• Neuropathies, including Guillain-Barre syndrome, metabolic neuropathies (diabetes, uremic), paraneoplastic or autoimmune.

• Neuromuscular junction disorders, including myasthenia gravis.

• Myopathies, including acute inflammatory myopathies and hyperkalaemic periodic paralysis.

Clinical features such as time of onset, sensory and sphincter involvement can help exclude many of these possibilities.

Treatment

Hyperkalaemia correction is based on several principles such as stabilisation of the myocardial membrane in order to prevent arrhythmias, shifting of potassium into the intracellular space and increasing potassium excretion.

Correction was then started in order to address all these mechanisms: calcium gluconate for myocardium stabilisation, insulin in dextrose and salbutamol for a rapid lowering of potassium with shifting into the intracellular space and placement of a urinary catheter with 100 mg of furosemide in order to resolve the obstruction and stimulate diuresis.

Tumour lysis syndrome was assumed, based on the clinical history and laboratory findings, and the patient started taking rasburicase.

Outcome and follow-up

Three hours after admission, the patient showed a good clinical response with partial return of limb movement and urinary output of 4500 cc since urinary catheterisation. Repeat blood gasses showed an improvement in hyperkalaemia (from 9.0 mmol/L to 7.8 mmol/L). After discussion with nephrology, dialysis was not started due to the favourable clinical and analytical response. At the 12-hour mark, the patient had a normal serum potassium level with complete normalisation of motor functions. He was later admitted to a surgical close-monitoring ward.

The patient recovered renal function during the hospitalisation period, with normal creatinine, 4 days after admission. Despite chemotherapy and radiotherapy, the masses proved unresectable due to extensive invasion of adjacent structures, and the patient was discharged from the hospital and continued chemotherapy and radiotherapy. The following month the patient developed intestinal obstruction and an ileostomy was performed. The patient passed away 3 months after the reported events.