Chairmans Hour

Christian Daniel U. Ang Maria Sueli P. Aplicador Lordan G. Carreon

May 30, 2012

General Data
Patient: MD Age/Sex: 19M Birthdate: June 3, 1992 Address: 1011-A Ciria St. Pandacan, Manila Contact Number: 0927-3162531 E-mail: None Occupation: Unemployed Date of Admission: May 3, 2012 Informant: Patient Reliability: Good

Chief Complaint
Nang-hihina ang aking mga balikat, hitat paa Weakness of Upper and Lower Extremities

History of Present Illness

Sudden weakness of UE and LE upon waking up described as difficulty in ambulating, difficulty in reaching out for objects Symptoms resolved gradually in app. 4-6 hours Weakness more pronounced on shoulders and hips (-) pain, trauma, dizziness, sensorium change, rigidity, sensory deficit, palpitations, weight loss Still able to perform activities of daily living No consult or medications

2 years PTA

History of Present Illness

Episode of weakness after a 2-hour bus ride Described as difficulty in standing up from his seat, pulling himself up and carrying his bag. (-) pain, dizziness, sensorium change, rigidity, sensory deficit, palpitations, weight loss Symptoms gradually resolved in app. 4-6 hours Still able to perform activities of daily living No consult or medications

6 months PTA

History of Present Illness

Another episode after a 1.5-hour taxi ride Described to be more severe (parang hindi na ako makagalaw) Can not ambulate alone (had to call his relative for Few hours support in disembarking) Can not perform ADLs alone (changing clothes, PTA toothbrush) Symptoms persisted for app. 6 hours, prompting ER consult

Past Medical History

Current Illnesses: None Previous Illnesses/Hospitalizations: None Previous Surgeries: None Known Allergies: None Previous Transfusions: None Immunizations: Unrecalled Current Medications: no diuretics no herbal supplements no diet pills no vitamins

Personal History
Diet: Mixed diet Smoking: 0.2 pack year smoker Illicit Drug Use: No use of illicit drug Recent Travel: Laoag City, Baguio City

Family History
(+) Hypertension Maternal, Paternal (+) Colon CA Maternal (-) Thyroid Disease (-) DM (-) Asthma

Social History
Source of Income: parents Primary caretaker: parents Family Relationships: good family relationship Residence: clean environment, well-ventilated house

Review of Systems (only the pertinent)

General:(-) weight loss, (-) fever, (-) headache, (-) dizziness Integumentary: (+) diaphoresis, (-) loss of sensation Respiratory:(-) dyspnea Cardiovascular: (-) chest pain Gastrointestinal: (-) vomiting, (-) diarrhea, (-) constipation Genitourinary: (-) frequency, (-) dysuria, (-) change in urine color Psychiatric: (-) anxiety, (-) depression

Physical Examination on Admission

General Survey: Conscious, coherent, wheelchair-borne, not in cardiorespiratory distress, not in pain Vital Signs: BP : 130/90 mm Hg (supine), PR : 68, reg, RR 17, Temp: 36.6C, O2 sat : 98% Wt: 90kg. Ht: 58 BMI: 31.14 Skin: Warm, no active dermatoses, no pallor, no jaundice, brownish striae on the abdomen, whitish striae on the knees Eyes: no ptosis, pink palpebral conjunctivae, anicteric sclera, pupils 2-3 mm ERTL Ears: no aural discharge, no tragal tenderness Nose: midline septum, no nasal tenderness and discharge, no alar flaring

Physical Examination on Admission

Mouth: dry buccal mucosa, no oral and palatal lesions, no gum bleeding Throat: tonsils not enlarged, non-hyperemic posterior pharyngeal wall Neck: supple neck, no supraclavicular retractions, no enlarged lymph nodes, no thyroid enlargement, trachea midline Respiratory: No chest wall deformities, symmetrical chest expansion, equal tactile and vocal fremiti, no adventitious breath sounds

Physical Examination on Admission

Cardiovascular: JVP 3.0 at 30, CAP rapid upstroke, gradual downstroke, adynamic precordium, apex beat at 5th LICS MCL, (-) heaves, thrills, and lifts, S1 louder than S2 at apex and S2 louder than S1 at base Gastrointestinal: Globular abdomen, normoactive bowel sounds, tympanitic, soft, non-tender, no masses, liver span 8cm, Traubes space non-obliterated Genitourinary: no CVA tenderness Extremities: no tenderness, no edema, full and equal pulses, no limitation of ROM

Neurological exam Mental Status: conscious, coherent, oriented Cranial Nerves:

CN I no anosmia CN II pupils 2-3mm ERTL CN III, IV, VI EOM intact, no ptosis CN V face sensory intact, can clench teeth CN VII no facial asymmetry, can close eyebrows CN VIII hearing intact CN IX, X uvula midline on phonation, (+) gag reflex CN XI can turn head against resistance CN XII tongue midline on protrusion

Motor: 3/5 both LE, 3/5 both UE Cerebellum: good finger-to-nose test, alternate pronation-supination test Sensory: intact Reflexes: (++) Meningeal signs:(-) nuchal rigidity

Salient Features
SUBJECTIVE
19 year old, male Episodic generalized weakness (quadriparesis) No other symptoms
(-) pain (-) dizziness (-) sensorium change (-) rigidity (-) sensory deficit (-) palpitations (-) weight loss No fatigue/change in urine color No intake of diuretics, diet pills

OBJECTIVE
Conscious, coherent, not in respiratory distress Normal vital signs BMI: 31.14 (obese) (-) signs of trauma (-) ptosis (-) limitation of ROM Motor: UE (3/5), LE (3/5) Cerebellum intact Sensory intact Reflexes (++)

What do you think is present in our patient?

Assessment
Causes of Episodic Generalized Weakness:

1. Electrolyte disturbance
(e.g. Hypokalemia, hyperkalemia, hypercalcemia, hypernatremia, hyponatremia)

2. Muscle Disorders
(impaired carbohydrate or fatty acid utilization)

3. Neuromuscular Junction Disorders

(myasthenia gravis, lambert-eaton syndrome)

4. CNS Disorders
(TIA of brain, multiple sclerosis)

Assessment
Causes of Episodic Generalized Weakness:

1. Electrolyte disturbance
(e.g. Hypokalemia, hyperkalemia, hypercalcemia, hypernatremia, hyponatremia)

2. Muscle Disorders
(impaired carbohydrate or fatty acid utilization)

3. Neuromuscular Junction Disorders

(myasthenia gravis, lambert-eaton syndrome)

4. CNS Disorders
(TIA of brain, multiple sclerosis)

Diagnostic Plans
Serum electrolytes imbalances could lead to weakness!
(Na, K)

Capillary Blood Glucose TSH, FT3, FT4 - hyperthyroidism could lead to weakness Urine Chemistry if there are renal losses

Thank You Chairman!

Blood Chemistry
Test Urea Nitrogen
May 3 Reference Range

9-23

Creatinine Sodium
Potassium Chloride Magnesium Ionized Calcium

0.5-1.2 141.00
1.79 LOW

137-147
3.8-5 98-110 1.6-2.59 1.12-1.32

Urine Chemistry
Test Creatinine-Urine Sodium - Urine May 3 82.83 34.00 LOW Reference Range 39-259 40-220

Potassium - Urine
Urine Osmolality

7.65
341.00

LOW
LOW

25-125
500-800

Capillary Blood Sugar

May 3 138 mg/dl

Based from the initial diagnostic procedures, we could say that our patient has

HYPOKALEMIA

How do we approach a patient with HYPOKALEMIA?

Algorithm depicting approach to Hypokalemia

Algorithm depicting approach to Hypokalemia

Urine Chemistry
Test Creatinine-Urine Sodium - Urine May 3 (10:50PM) 82.83 34.00 LOW Reference Range 39-259 40-220

Potassium - Urine
Urine Osmolality

7.65
341.00

LOW
LOw

25-125
500-800

Algorithm depicting approach to Hypokalemia

Remember: Potassium-Urine 7.65 mmol/L

Our patients cause of hypokalemia is due to EXTRARENAL LOSS

ABG
May 3 (3:30PM) pH pCO2 p02 7.455 36.6 mmHg 94.1 mmHg HCO3 02 Sat BE TC02 Temperature Fi02 BP 37.0 21.0% 755.3 mmHg 02CT BB SBF AaD02 a/A R1 May 3 (3:30PM) 25.7 mmol/L 97.4% 2.8 mmol/L 26.8 mmol/L 20.6 vol% 50.8 mmol/L 2.5 mmol/L 10.8 mmHg 0.90 0.1

Algorithm depicting approach to Hypokalemia

Remember: ABG pH = 7.455

Algorithm depicting approach to Hypokalemia

In our Patient, these are the possible causes of Hypokalemia: - Remote Diuretic Use - Remote Vomiting or Stomach Drainage - Profuse Sweating***

After all the diagnostic procedures requested, our assessment is:

Hypokalemic Paralysis
due to excessive sweating

Now that we know what is wrong with our patient, we should treat him in our ward!

Management
Therapeutic Goals: Correct the K deficit (potassium replacement) Our patients serum K level: 1.79 mmol/L

Potassium Deficit = Desired - Actual = 3.5 1.79 = 1.71 meq

Management
Potassium Deficit = Desired - Actual = 3.5 1.79 = 1.71 meq

1 durule = 0.1 meq increase 40 meqs KCl IV = 0.4 meq increase

Given to our patient:

(2 bags) IV Potassium Chloride drip = 0.4 x 2 = 0.8 Initially given 2 kalium durules at the ER Then 1 durule q8 for 3 days = 0.2 + (0.1 x 3 x 3) = 1.1 Total K replaced = 0.8 + 1.1 = 1.9 meqs (out deficit was 1.71)

Our patient was asymptomatic by the third day, his last serum K level was 3.66 meq/L
It was a success!

Management
Medications:
Potassium Chloride** (Kalium Durule) - Preparation of choice - More rapid correction and metabolic alkalosis
Potassium HCO3 and Citrate
More appropriate in hypokalemia associated with chronic diarrhea or RTA

Management
Medications:
Intravenous Potassium Chloride** - Only for severe hypokalemia - Unable to take anything by mouth - Hyperkalemia-prone - used judiciously, close observation!

Thank You!

Lets Discuss HYPOKALEMIA!

IF NEEDED ONLY

Hypokalemia
Plasma K concentration <3.5 mmol/L Results from: I. Decreased Intake II. Redistribution into cells III. Increased Loss

I. Decrease Intake
A. Starvation - diminished intake is seldom the sole cause - amount of K in the diet almost always exceeds that excreted in the urine B. Clay ingestion - binds dietary K and iron

II. Redistribution into Cells

A. Acid-Base Metabolic Alkalosis occurs as a result K redistribution as well as excessive renal K loss B. Hormonal Insulin stimulation of Na-H antiporter and Na-K-ATPase B2-Adrenergic agonists induce cellular uptake of K and promote insulin secretion C. Anabolic State K shift into cells (following rapid cell growth) RBC production WBC production Frozen Blood transfusion (lost K during storage)

III. Increased Loss

A. Non-Renal Gastrointestinal loss diarrhea, VIPomas, laxative abuse Integumentary loss excessive sweating B. Renal Increased Distal flow diuretics, osmotic diuresis Increased secretion of potassium mineralocorticoid excess - Adrenal adenoma (Conns syndrome) and hyperplasia - Hyperreninemia (renal K wasting seen in renovascular HPN)

Hypokalemia: Clinical Manifestations

Symptoms occur when plasma K concentration is <3 mmol/L Common: Fatigue, myalgia, muscular weakness of LEs

Severe: progressive weakness, hypoventilation, paralysis

Increased risk of rhabdomyolysis Increased risk of paralytic ileus

Hypokalemia: Clinical Manifestations

ECG changes:
Flattening/inversion of T-waves Prominent U-waves ST-segment depression Prolonged QU-interval* Prolonged PR interval Widening of the QRS complex

*Increased risk of VENTRICULAR ARRHYTMIAS (especially in patients with MI and LVH)

Hypokalemia: Clinical Manifestations

Acid-Base disturbances K depletion results in Intracellular Acidification and an increase in net acid excretion or production of new HCO3 Leads to METABOLIC ALKALOSIS! Consequence of: Enhanced proximal HCO3 reabsorption Increased renal ammoniagenesis Increased distal H excretion

What is TTKG?
Trans-Tubular Potassium Gradient

An index reflecting the conservation of K in the CCD Useful in diagnosing the causes of Hypo/Hypo-K

Only NICE TO KNOW in this case

Algorithm depicting approach to Hypokalemia

What is TTKG?
Trans-Tubular Potassium Gradient

An index reflecting the conservation of K in the CCD Useful in diagnosing the causes of Hypo/Hypo-K TTKG = (Urine K x Serum Osm) / (serum K x urine osmol) = (7.65 x 293) / (1.79 x 341) = 2241.45/610.39 TTKG = 3.67 Serum Osm = 2Na + (Glucose/18) + (BUN/2.8)
= 282 + 7.67 + 3.58 Serum osm = 293

We can NOT use TTKG in our patient! In the algorithm, it is only <2 or >4

TTKG

Only NICE TO KNOW in this case