Chairman’s Hour

Christian Daniel U. AngMaria 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, hita’t paa’Weakness of Upper and Lower Extremities

History of Present Illness

2 years PTA

• 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

History of Present Illness

6 months PTA

• 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

History of Present Illness

Few hours PTA

• 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

support in disembarking)• Can not perform ADLs alone (changing clothes,

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 diureticsno herbal supplementsno diet pillsno 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: 36.6°C, O2 sat : 98%

• Wt: 90kg. Ht: 5’8” 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, Traube’s 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 FeaturesSUBJECTIVE• 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?

AssessmentCauses 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)

AssessmentCauses 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 ChemistryTest May 3 Reference

Range

Urea Nitrogen 9-23

Creatinine 0.5-1.2

Sodium 141.00 137-147

Potassium 1.79 LOW 3.8-5

Chloride 98-110

Magnesium 1.6-2.59

Ionized Calcium 1.12-1.32

Urine Chemistry Test May 3 Reference

RangeCreatinine-Urine 82.83 39-259

Sodium - Urine 34.00 LOW 40-220

Potassium - Urine 7.65 LOW 25-125

Urine Osmolality 341.00 LOW 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 May 3

(10:50PM)Reference

RangeCreatinine-Urine 82.83 39-259

Sodium - Urine 34.00 LOW 40-220

Potassium - Urine 7.65 LOW 25-125

Urine Osmolality 341.00 LOw 500-800

Algorithm depicting approach to Hypokalemia

Remember:Potassium-Urine 7.65 mmol/L

Our patient’s cause of hypokalemia is due to EXTRARENAL LOSS

ABGMay 3 (3:30PM)

pH 7.455

pCO2 36.6 mmHg

p02 94.1 mmHg

Temperature 37.0

Fi02 21.0%

BP 755.3 mmHg

May 3 (3:30PM)

HCO3 25.7 mmol/L

02 Sat 97.4%

BE 2.8 mmol/L

TC02 26.8 mmol/L

02CT 20.6 vol%

BB 50.8 mmol/L

SBF 2.5 mmol/L

AaD02 10.8 mmHg

a/A 0.90

R1 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 patient’s 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!

Let’s DiscussHYPOKALEMIA!

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 CellsA. 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 ½ K during storage)

III. Increased LossA. 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 (Conn’s 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

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

Serum Osm = 2Na + (Glucose/18) + (BUN/2.8)= 282 + 7.67 + 3.58

Serum osm = 293

TTKG

Only NICE TO KNOW in this

case