26-Year-Old Man Regains Mobility After Severe Muscle Weakness Caused by Life-Threatening Low Potassium Levels

In this medical case study, we explore the journey of a 26-year-old male patient who experienced sudden and alarming muscle paralysis in both legs—later diagnosed as severe hypokalemia (low potassium levels). Prompt diagnosis and aggressive treatment not only reversed his symptoms but also restored full mobility within just three days. While the condition originated from an unexpected source—a routine clinic injection—the outcome highlights the importance of recognizing subtle hormonal side effects and electrolyte imbalances.

Understanding Hypokalemia: A Silent Threat to Neuromuscular Function

Hypokalemia, defined as abnormally low levels of potassium in the bloodstream, can lead to significant neuromuscular dysfunction. Potassium plays a critical role in nerve signaling and muscle contraction, including the heart and skeletal muscles. When levels drop below normal—typically under 3.5 mmol/L—patients may experience weakness, fatigue, tingling sensations, or even complete paralysis. In extreme cases like this one, with serum potassium measured at a dangerously low 1.5 mmol/L, immediate intervention is essential to prevent cardiac complications.

Patient Profile & Initial Presentation

Age: 26 yearsGender: MalePrimary Conditions: Acute hypokalemia, acute tonsillitisHospital: Second Affiliated Hospital of Harbin Medical UniversityTreatment Duration: 3-day inpatient careTherapy Approach: Intravenous potassium replacement via subclavian vein, oral potassium supplements, antibiotic therapy

The patient arrived at the emergency department via ambulance after experiencing progressive numbness, heaviness, and loss of strength in both lower limbs over a two-hour period. By the time he reached the hospital, he was unable to move his legs independently, though he retained control over bladder and bowel functions. He was wheeled into the ward showing signs of distress and profound muscle weakness—clinical assessment revealed grade 0 muscle strength in both lower extremities.

Uncovering the Root Cause: From Fever to Paralysis

A detailed medical history uncovered a crucial clue: the day before symptom onset, the patient had visited a local clinic for fever and sore throat. There, he received intramuscular injections of dexamethasone sodium phosphate and intravenous levofloxacin sodium chloride—common treatments for inflammation and bacterial infection. However, it was the corticosteroid (dexamethasone) that likely triggered a dangerous shift in potassium metabolism.

Corticosteroids are known to increase cellular uptake of potassium, effectively pulling it out of circulation and into cells, which leads to transient but potentially severe hypokalemia. The patient denied excessive consumption of sugary drinks or other risk factors, making steroid-induced potassium depletion the most plausible explanation.

Differential Diagnosis and Ruling Out Neurological Emergencies

Given the sudden onset of leg paralysis, neurological conditions such as Guillain-Barré syndrome, spinal cord compression, or stroke were initially suspected. To rule these out, a head CT scan was performed immediately upon admission—it showed no abnormalities. This helped narrow the focus to metabolic causes rather than structural brain or spinal issues.

A blood gas analysis delivered the definitive answer: serum potassium level was critically low at 1.5 mmol/L, confirming the diagnosis of acute hypokalemia. With this result, the treatment team shifted priorities toward rapid potassium correction while managing concurrent infections.

Comprehensive Treatment Strategy: Rebuilding Strength Step by Step

The treatment plan combined three key components:

• Intravenous potassium chloride infusion through a central venous line (subclavian vein)
• Oral potassium supplementation using bismuth potassium citrate granules
• Antibiotic therapy with amoxicillin sodium for acute bacterial tonsillitis

Physical examination during admission revealed bilateral tonsillar swelling (Grade II), pus-covered surfaces, and elevated white blood cell count (14.1 x 10⁹/L) with 78.8% neutrophils—clear indicators of active infection. Penicillin skin testing was conducted and came back negative, allowing safe initiation of amoxicillin therapy.

Overcoming Challenges in Potassium Replacement Therapy

Initially, peripheral IV potassium administration caused intense vein irritation and pain, despite slowing the drip rate and switching infusion sites. Due to the severity of hypokalemia and the urgent need for high-dose potassium, the medical team proposed central venous access. After discussing risks and benefits with the family, consent was obtained, and a subclavian vein catheter was placed successfully.

This approach allowed faster, safer delivery of concentrated potassium solutions without vascular discomfort—critical for avoiding delays in recovery.

Rapid Recovery and Clinical Outcomes

The results were remarkable:

Within three hours of starting central venous potassium replacement, the patient regained voluntary movement in his toes and could slide his legs across the bed surface. Blood tests showed potassium rising to 2.5 mmol/L. Six hours later, muscle strength improved to Grade IV, enabling independent limb movement, and serum potassium reached 3.8 mmol/L—within the normal range.

The antibiotic treatment also took effect quickly. Tonsil pain diminished significantly, exudates cleared, and follow-up blood work showed normalization of white blood cell counts. Thyroid function tests were unremarkable, ruling out endocrine-related causes of potassium imbalance.

After three days of close monitoring and tailored therapy adjustments—including tapering IV potassium and transitioning fully to oral supplements—the patient achieved full functional recovery. He walked out of the hospital without assistance, with all vital signs and lab values restored to baseline.

Post-Discharge Guidance for Long-Term Wellness

To support sustained recovery and prevent recurrence, the following lifestyle and dietary recommendations were provided:

• Eat potassium-rich foods: Lean meats (beef, pork), bananas, dates, spinach, avocados, potatoes, and beans
• Avoid high-sugar meals: Sweets like cakes, pastries, and mooncakes can worsen insulin spikes that drive potassium into cells
• Practice frequent small meals: Helps stabilize blood sugar and electrolyte balance
• Take medication with food: Bismuth potassium citrate may cause mild stomach upset; taking it after eating reduces gastrointestinal side effects
• Avoid alcohol and smoking: Both can interfere with nutrient absorption and immune function

Patients are advised to seek medical attention immediately if they experience muscle cramps, palpitations, fatigue, or weakness—especially after receiving steroid injections or antibiotics.

Clinical Insights: Learning from a Steroid-Induced Crisis

This case underscores a frequently overlooked complication of glucocorticoid therapy: acute hypokalemia. Dexamethasone, although effective for reducing inflammation, alters electrolyte dynamics by enhancing sodium retention and potassium excretion through renal pathways, compounded by increased cellular uptake.

While many patients experience only mild symptoms that resolve spontaneously, clinicians must remain vigilant—particularly when steroids are combined with glucose-containing fluids, which stimulate insulin release and further drive potassium into cells.

Monitoring During IV Potassium Infusion

Safety is paramount during potassium repletion. Continuous ECG monitoring is recommended to detect early signs of hyperkalemia (such as peaked T-waves or arrhythmias), especially when administering high concentrations via central lines. Frequent blood draws ensure steady, controlled correction—avoiding the "overshoot" that could trigger life-threatening cardiac events.

In conclusion, this case demonstrates how timely recognition of drug-induced metabolic disturbances can transform a potentially catastrophic event into a successful recovery story. Awareness, prompt diagnostics, and targeted interventions saved this young man's mobility—and possibly his life.