Hypokalemic Paralysis from Distal Renal Tubular Acidosis (Type-1)

Silvera Samson Raj1, Aslesha Vijaay Sheth2

3rd year Emergency Resident, Kauvery Hospital, Chennai

Clinical lead – Department of Emergency Medicine, Kauvery Hospital, Chennai

Case Presentation

Chief Complaints

A 39 Years gentleman with no comorbid, NKDA and with a chief complaints of :

  1. Tightness in bilateral calf muscles 2 weeks ago that settled on taking rest
  2. Bilateral lower limb cramps 3 days ago, treated in outside clinic with intravenous fluids
  3. Ascending weakness in both legs, thighs, hips and low back initially gradually worsened involving both hands since last 2 days
  4. Mild breathing difficulty since morning

Patient was initially treated elsewhere and brought here for further Management.

Investigations done outside showed CPK – 491, Na+ – 149, K+ – 3, Cl – 115, urea – 36, creatinine – 1.6.

No past medical/surgical history.

On examination (1:45 PM)

Conscious, oriented, afebrile, hydration-fair, no PICCLE. Vitals:

  1. PR – 78/min
  2. BP – 160/100 mmHg
  3. RR – 18/min
  4. SpO2 – 98% RA
  5. Temp – 97.80 F
  6. CBG – 136 mg/dl
  7. GCS – 15/15

Systemic Examination

CVS – S1S2 +, no murmur, JVP – normal.

RS – B/L air entry equal, NVBS, SBC – 30.

PA – Soft, non- tender, bowel sounds sluggishly heard. CNS: UMN- intact, EOM- full, B/L pupil 3mm-ERTL




Power UL 2/5 2/5
Power LL 1/5 1/5
Tone Hypotonic Hypotonic
DTR Absent Absent
Plantar Mute Mute
Sensory Intact Intact

Primary Management

  1. After Neuro opinion, on suspicion of GBS,  started on IVIG around 4pm.
  2. Around 5pm patient had worsening breathing difficulty with desaturation around 89% RA – started on 2L O2 NP.
  3. At 7pm due to further desaturation (80% with O2) and poor respiratory effort, pt electively intubated in ER.
  4. Medipack was sent and reports awaited. .

Differential diagnoses

  1. GBS
  2. Ascending polyneuritis, Miller Fischer syndrome, Stroke
  3. Neuro muscular junction disorder like MG, botulism
  4. Spinal cord disorder like Transverse Myelitis, compression myelopathy
  5. Myositis
  6. Metabolic and thyrotoxic myopathies
  7. Heavy metal toxicity
  8. Infection
  9. Hypokalemia related weakness

At 8:30pm pt had a sudden drop in heart rate (HR=30/min),

BP=70/50mmHg) – treated with Inj. Atropine 0.6mg IV stat – HR picked up to 86/min.

Immediate ABG and ECG done.

Arterial Blood Gas

PH 7.28
PCO2 24 mmHg
PO2 22O mmHg
Na+ 141 mmol/L
K+ 0.9 mmol/L
Cl- 113 mmol/L
Lactate 1.4 mmol/L
hco3 11.3 mmol/L
SO2 97%
AG 18

Initial ECG


Post correction ECG


Lab Investigations

Complete Blood Count

Hb 16.8
WBC 18300
Platelet 209000
ESR 10
Neutrophil 91.4
Lymphocyte 6.1
Monocyte 2.5
Basophil 0

Renal Function Test

Urea 55.7
Creat 2.03
Sodium 143.4
Potassium 1.4
Chloride 114.9
Bicarb 16
Uric acid 5.96

Urine Routine

pH 7
Specific gravity 1.01
Glucose Neg
Protein Trace
Blood +++
Ketone Neg
Nitrite Neg
Pus cells 10-12
RBC 2-4
Sodium spot 105
Potassium spot 13.8
Creatinine spot 22.26
Chloride spot 109

Serology: Negative


Nerve Conduction Study

  1. Sensory responses are well preserved.
  2. Motor responses are reduced in amplitude in upper, lower limbs motor response delay in distal motor latencies with reduction in conduction velocity.
  3. Findings point to motor predominant neuropathy mixed axonal and demyelinating features

Secondary management

  1. With the clinical picture and labs we have, our DD narrowed down to:
  1. GBS
  2. Hypokalemia related weakness
  3. Stroke
  4. Transverse myelitis, compression myelopathy
  1. Patient started on Inj. KCl 60 mEq in 100ml NS over 1 hour followed by 60MEq in 500ml RL @150ml/hr.
  2. Inj. Sodium Bicarbonate 100ml in 5% Dextrose @300ml/hr.
  3. In view of HR=220/min, started on Inj.Esmolol 2mg IV stat followed by 4ml/hr infusion.
  4. Pt condition improved the next day morning, hence extubated and weaned off from other supports

Other Investigations

USG Abdomen: Suggestive of medullary nephrocalcinosis.


Repeat NCS: No evidence for generalised peripheral neuropathy.


MRI Brain: No evidence of haemorrhages, infarcts, mass lesion or demyelination seen.



Hypokalemia classification and management in ER

Mild: 3-3.4 mmol/L


  1. S Oral KCl syrup.
  2. S Potassium sparring diuretics if on diuretic therapy.

Moderate: 2.5-2.9 mmol/L


  1. Inj.Kcl 20 mEq in 100ml NS or 500ml NS/RL over 4-5 hours.

Severe: <2.5 mmol/L


  1. S Inj.Kcl 40mEq in 100ml NS or 500ml NS/RL over 4-5 hr.

How will you manage cardiac/peri arrest patient secondary to severe hypokalemia?

In case of cardiac arrest or life threatening arrhythmia secondary to hypokalemia:

  1. S Inj. KCL 20mEq IVI over 20 – 30mins
  2. S Repeat dose if needed

Hypokalemic Periodic Paralysis

  1. Condition that causes episodes of extreme muscle weakness.
  2. Episodes involve temporary inability to move muscles in the arms and legs.
  3. Attacks causes severe weakness or paralysis which are reversible with appropiate treatment.
  4. Early recognition is vital as hypokalemia can lead to dangerous VT and sudden cardiac arrest

Renal Tubular Acidosis

  1. Renal tubular acidosis (RTA) is acidosis and electrolyte disturbances due to impaired renal hydrogen ion excretion (type 1), impaired bicarbonate resorption (type 2), or abnormal aldosterone production or response (type 4). (Type 3 is extremely rare and is not discussed.)
  2. ABG shows normal anion gap metabolic acidosis.
  3. Patients may be asymptomatic, display symptoms and signs of electrolyte derangements, or progress to chronic kidney disease.
  4. Diagnosis is based on characteristic changes in urine pH and electrolytes in response to provocative testing.
  5. Treatment corrects pH and electrolyte imbalances using alkaline agents, electrolytes, and rarely drugs.

Type 1 Distal RTA

  1. Impaired Hydrogen Ion Secretion
  2. Urine pH > 5.5
  3. Hypokalemia
  4. Renal stones

Type 2 Proximal RTA

  1. Impaired bicarbonate reabsorption
  2. High urine ph initially later < 5.5
  3. Hypokalemia

Type 4 Hyperkalemic RTA Decreased Aldosterone

  1. Secretion or aldosterone
  2. Resistance
  3. Urine pH < 5.5
  4. Hyperkalemia

Classification and Interpretation






2 low normal <5.5 No
1 (ODD)



low high >5.5 Yes
4 more normal <5.5 No


  1. Hypokalemia is a commonest electrolyte imbalance we see in our day to day routine in ER.
  2. In this patient, the cause of hypokalemia is distal renal tubular acidosis (type-1).
  3. Hypokalemic periodic paralysis is not uncommon but easily misdiagnosed.
  4. Checking for any reversible causes and treating it first helps both patient and physicians

Dr. Silvera Samson Raj

Emergency Resident


Dr. Aslesha Vijaay Sheth

Clinical lead – Department of Emergency Medicine