Bondoc.Borela.Buenaventura.Buhat.Calaoagan. Carilo.Casi.Castano.Celino.Francisco.Garcia

1. Bondoc.Borela.Buenaventura.Buhat.Calaoagan. Carilo.Casi.Castano.Celino.Francisco.Garcia

2. Identifying data • M.I is 35 y/o • Female • Married • Filipino • Roman Catholic • Admitted for the first time at UERMMMC

3. Chief Complaint • Generalized body weakness of 12 hours duration

4. History of Present Illness

5. Past Medical History • Hypertension- diagnosed 7 years ago • Rx: Amlodipine 10 mg/tab 1 tab OD, Losartan 50 mg/tab 1 tab OD • Surgery: • 1999: Right oophorectomy • 2008: total abdominal hysterectomy with left oophorectomy • 2 years PTA, admitted due to similar episode of weakness • No history of DM, thyroid, kidney, lung, heart disorders

6. Family History • Father- DM type 2 • Mother- hypertension • No family history of heart, lung, kidney and connective tissue disorders Personal and Social History • Unremarkable

7. Physical Exam • Awake, conscious, coherent, stretcher bound • Vital signs: BP is 150/100, HR- 76 bpm, RR-18 cpm, Temperature is 37.1 ˚C • Remarkable findings: grade 3/5 pulses, Muscle strenght: 3/5 both upper extremities 1/5 on both lower extremites • Normotonic, normoreflexive, intact sensation, other neurological exams are normal.

8. Bilateral Weakness Serum K+ Neurologic Neuromuscular Junction Myopathies >4.3 mmol/L <3.4 mmol/L CBC <50,000 WBC count >50,000 WBC count Pseudohypokalemia Recent insulin, B-adrenergic, theophyline use, or, more rarely, anabolic stimulus or family history suggestive of hypokalemic periodic paralysis Redistribution or hypokalemic periodic paralysis Yes No Skin, GI or Renal K Loss ABG Acidosis Alkalosis Urine K+ <20 mEq K/24 hrs >20 mEq K/24 hrs Recent diuretic use? No Yes Probable diuretic-induced hypokalemia CHF, hepatic insufficiency, nephrotic syndrome or renal artery stenosis Yes Probable secondary hyperaldosteronism RTA, DKA or ureterosigmoidostomy Low No Serum bicarbonate? No Hypomagnesemia? Random Urine K/C ratio Yes Normal or High Hypomagnesemia induced hypokalemia Blood Pressure >1.5 <1.5 Thyrotoxic PP Elevated High Low TSH >4.25 uLU/mL FT4: >1.7 ng/L TSH <0.34 uLU/mL FT4 <0.8 ng/L PRA and PAC High PAC Low PRA Both High Both Low Primary Aldosteronism CAH Cushing Syndrome Liddle Syndrome RVH, COA, RST

9. Bilateral Weakness • Neurologic • Altered mental status • Signs of UMN/LMN • Sensory deficit • Autonomic involvement • Neuromuscular Junction • Bulbar signs • Fatigability • Myopathies • All limbs involved • No sensory involvement • No autonomic involvement

10. Bilateral Weakness Neurologic Neuromuscular Junction Myopathies Serum K+ >4.3 mmol/L <3.4 mmol/L

11. CBC Pseudohypokalemia <50,000 WBC count >50,000 WBC count Recent insulin, B-adrenergic, theophyline use, or, more rarely, anabolic stimulus or family history suggestive of hypokalemic periodic paralysis Redistribution or hypokalemic periodic paralysis Yes No Skin, GI or Renal K Loss ABG Acidosis Alkalosis Urine K+ <20 mEq K/24 hrs >20 mEq K/24 hrs Recent diuretic use? No Yes Probable diuretic-induced hypokalemia CHF, hepatic insufficiency, nephrotic syndrome or renal artery stenosis Yes Probable secondary hyperaldosteronism RTA, DKA or ureterosigmoidostomy Low No Serum bicarbonate? No Hypomagnesemia? Random Urine K/C ratio Yes Normal or High Hypomagnesemia induced hypokalemia Blood Pressure >1.5 <1.5 Thyrotoxic PP Elevated High Low TSH >4.25 uLU/mL FT4: >1.7 ng/L TSH <0.34 uLU/mL FT4 <0.8 ng/L PRA and PAC High PAC Low PRA Both High Both Low Primary Aldosteronism CAH Cushing Syndrome Liddle Syndrome RVH, COA, RST

12. Differentials Diagnoses

16. Primary Aldosteronism Bilateral Adrenal Hyperplasia Aldosterone Secreting Adenoma CT scan

17. Primary Impression • Hypokalemia secondary to Primary Aldosteronism (Conn’s Syndrome)

18. Why rule in Hypokalemia? • Acute Generalized weakness • Absence of UMN and LMN signs, Sensory and Autonomic Involvement, Bulbar signs and Fatigability. • Marked decrease in K+ level (1.5mmol/L)

19. Definition of Hypokalemia • Plasma K+ concentration <3.5 mmol/L • May be due to: • Decreased net intake • Shift of K+ into cells • Increased net loss

20. Clinical Manifestations of Hypokalemia • Usually asymptomatic • Unless plasma K+ concentration <3 mmol/L • Fatigue, myalgia, muscular weakness of the lower extremities • Severe Hypokalemia → progressive weakness, hypoventilation and complete paralysis

21. Occurrence of Metabolic Alkalosis • High pH (7.56) • Low pCO2 (32) • High HCO3 (28.7) • Result of K+ redistribution + excessive renal K+ loss • K+ depletion → intracellular acidification →increase HCO3 production

22. Primary Hyperaldosteronism (Conn’s Syndrome)

23. Why rule in Primary Hyperaldosteronism? • Triad of Hypertension, Hypokalemia, and Metabolic Alkalosis • Elevated BP upon admission • Diagnosed with HTN 7 years ago • Poor compliance to maintenance medications • Hypokalemia and Metabolic Acidosis on lab tests

24. Primary Hyperaldosteronism • Syndrome associated with hypersecretion of adrenal mineralocorticoid Aldosterone • Accounts for 5-10% of hypertension cases • Peak incidence → 30-60 years old

25. Pathophysiology • Cellular uptake of K+ • Aldosterone → inc. Na+-K+ ATPase] → inc. transport of K+ into intracellular space • Regulation of Renal K+ transport • Aldosterone →inc. Apical Na conductance, basolateral Na+-K+ ATPase activity, and electrogenic Na absorption in the collecting tubules → K+ movement from intracellular to luminal fluid

26. Excessive aldosterone • increased sodium retention • decreased plasma renin • Increased renal potassium excretion →hypokalemia

27. Clinical Manifestations • Hypokalemia • Muscular weakness • K+ depletion in the muscle cell membrane • Paresthesias • Headache • Polyuria • Polydipsia • Moderate hypertension (diastolic) • Due to inc. Na reabsorption

28. Plasma Renin Activity (PRA) Plasma Aldosterone Concentration (PAC) • Primary Hyperaldosteronism is consistent with: • ↓PRA (baseline-12.69 ng/dL; post-12.36 ng/dL) • ↑PAC (<0.1 ng/mL/hr),

29. Diagnostics • CT Scan

30. Course in the Ward • Day of Admission • BP: elevated at 150/100mmHg • Inability to move both lower extremities • CBC • ↓ WBC count (13,100/L) with neutrophil predominance in absolute count • Serum electrolytes • ↓ potassium (1.5mmol/L) • Albumin & BUN: normal

31. Course in the Ward • Day of admission • Uric acid: ↑ (22 umol/L) • Creatinine: ↑ (100 umol/L) • Urine electrolytes •  potassium (9.2 mmol/l) • ABG • ↑ pH (7.56) and HCO3 (28.7mmol/L) • ↓ pCO2 (32mmHg)

32. Course in the Ward • Day of admission • FBS: normal • Lipid profile: normal • Urinalysis • Few bacterial and epithelial cells • CXR: clear • IV potassium chloride drip was started • Thyroid function test was requested

33. Course in the Ward • Day 2-3 • BP : 160/100mmHg • Movement of both legs from side to side • Gradual ↑ of potassium to 2.4mmol/L (day 3) • Thyroid function test: normal TSH and fT4 • Plan: saline suppression test when potassium level becomes normal

34. Course in the Ward • Day 4-5 • Able to walk around the room without assist • Serum potassium: 4.7mmol/L • IV potassium  oral • Saline suppression test • Baseline plasma renin activity and aldosterone  2L IV saline infused over 4 hours  plasma aldosterone

35. Course in the Ward • Day 4-5 • BP : 200/100mmHg • spironolactone 25mg/tab, 1 tablet BID and felodipine10mg/tab, 1 tablet OD • Dicharged with plans for follow-up • Plasma renin and aldosterone results after 2 weeks

36. Follow-up • BP maintained at 100-120/70-80mmHg • No recurrent weakness • Saline suppression test • ↑ baseline aldosterone: 12.69ng/dL • ↑ aldosterone post-infusion: 12.36ng/dL • ↓ plasma renin activitiy: <0.1ng/mL/hr

37. Follow-up • Abdominal CT scan requested • Hypodense enhancing nodule, measuring 9.9 x 7.6 x 11.7mm, at the lateral limb of the left adrenal gland • Right adrenal gland unremarkable • No other abnormalities in the pre-contrast, arterial, portal venous and wash-out phases • Liver, pancreas and gallbladder are unremarkable • Referral to surgery

38. Management • Control of hypertension and aldosterone level • Potassium supplementation • Abdominal CT scan • Adrenalectomy • Laparoscopic vs. open surgery • Complications • Prognosis

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