Group A2-a Alegre.Almora.Alonzo.Amaro.

 Name: H.N.  Age: 51  Gender: Female  Citizenship: Filipino  Chief Complaint: Persistent vomiting 2

3 2 days PTA Headache, body malaise, nausea and vomiting -vomited 3x per day, 50ml per episode (approximately of 150ml/day) ADMISSION 1 week PTA Fever, Dysuria, Urgency -Self-medicated w/ Paracetamol and antibiotics (unknown) that relieved the fever; no consult was done

Hypertension (1999) maintained on telmisartan + hydrochlorothiazide 40 mg / 12.5 mg OD for 1 month; Previously prescribed with Amlodipine but developed bipedal edema. Poorly controlled. – Usual BP 130/80. 4

 Non smoker  Non alcoholic beverage drinker 5

 Patient is weak looking and wheelchair borne  Poor skin turgor, dry mouth and tongue, dry axilla  JVP<5cm H2O at 45 degrees 6 BP: 120/180 (supine); 90/60 (sitting) HR: 90 bpm, reg (supine); 105 bpm, reg (sitting) Weight: 50 kg (usual wt. = 53kg) Note: (not given) Respiratory Rate, Height, Temperature

SUBJECTIVE  51 y/o F  History of vomiting (150ml/day)  History of fever, dysuria and urgency  Medications used (HCTZ and telmisartan)  History of nausea, body malaise, headache OBJECTIVE  Weak looking and wheelchair borne  Orthostatic hypotension  Possible weight loss  Poor skin turgor, dry mouth and tongue, dry axilla

Hypovolemia secondary to dehydration to consider electrolyte imbalance

Complete Blood Count Hemoglobin132 mg/dl ( mg/dl)Normal Hematocrit0.35 ( )Low WBC12.5 (4.5-10)High Neutrophils0.88 ( )High Lymphocytes0.12 ( )Low Blood Chemistry BUN22 mg/dl (8-23 mg/dL)Normal Serum Creatinine0.9 mg/dl ( mg/dl)High Plasma Sodium123 meq/L ( meq/L)Low Plasma Potassium3.7 meq/L ( meq/L)Normal Chloride71 meq/L ( meq/L)Low Glucose98 mg/dl ( mg/dl)Normal

Urinalysis ColorYellow, slightly turbidNormal pH6.0Normal Specific gravity1.020Normal Urinary Sodium100 meq/L (<20 meq/L) Albumin and sugar(-)Normal Pus cells10-15/hpfHigh Hyaline casts5/hpfHigh RBC2-5/hpfNormal Arterial Blood Gas pH7.3 ( )Low pCO235 mm Hg (35-45 mm Hg)Normal HCO318 (22-26 meq/L)Low Anion Gap34 (<12)High

 History  Physical examination - assess ECF volume status and effective circulating arterial volume  Laboratory - plasma osmolality, urine osmolality - urine Na and K concentrations

Plasma osmolality highnormallow Hyperglycemia mannitol Hyperproteinemia Hyperlipidemia Bladder irrigation Max volume of max dilute urine (<100 mosmols/kg) ECF volume Primary polydypsia Reset ormostat Yes No

normalincreaseddecreased ECF volume Heart failure Hepatic cirrhosis Nephrotic syndrome Renal insufficiency SIADH Exclude hypothyroidism Exclude adrenal insufficiency Urine [Na] < 10 mmol/L>20 mmol/L Extrarenal Na loss Remote diuretic use Remote vomiting Na-wasting nephropathy Hypoaldosteronism Diuretic vomiting

Hypovolemic hyponatremia w/ uncompensated hypochloremic metabolic acidosis secondary to dehydration (ECF volume contraction)

 Primary Sodium Loss (secondary water gain)  Integumentary loss: ▪ Increased insensible loss during febrile illness  Gastrointestinal loss: ▪ Vomiting  Renal loss: ▪ Diuretics ▪ Osmotic diuresis

 Gastrointestinal Loss  Vomiting (high H+ ion loss)  Decreased intake of fluids (w/ nausea) or replaced by inappropriately hypotonic fluids, such as tap water, half-normal saline, or dextrose in water  Skin/Respiratory  Insensible losses (normally 500 ml/d) increases during febrile illness leading

 Diuretics  inhibit specific pathways of Na + reabsorption along the nephron with a consequent increase in urinary Na + excretion  Osmotic Diuresis  Enhanced filtration of non-reabsorbed solutes, such as glucose or urea, can also impair tubular reabsorption of Na + and water

 ACE inhibitors  Inhibit the RAAS system  decreased sodium retention  Inhibit release of ADH  decreased H2O retention  Thiazides  “diuretic-induced hyponatremia”  Leads to Na and K depletion and AVP-mediated H2O retention

 Hypovolemic hyponatremia develops as sodium and free water are lost and replaced by inappropriately hypotonic fluids, such as tap water, half- normal saline, or dextrose in water. Sodium can be lost through renal or nonrenal routes. Nonrenal routes include GI losses, excessive sweating, third spacing of fluids (eg, peritonitis, pancreatitis, burns), and the cerebral salt-wasting syndrome.  Excess fluid losses (eg, vomiting, diarrhea, excessive sweating, GI fistulas or drainage tubes, pancreatitis, burns) that have been replaced primarily by hypotonic fluids  Acute or chronic renal insufficiency in which patient may be unable to excrete adequate amounts of free water  Salt-wasting nephropathy  Cerebral salt-wasting syndrome seen in patients with traumatic brain injury, aneurysmal subarachnoid hemorrhage, and intracranial surgery  Prolonged exercise in a hot environment, especially in patients who hydrate aggressively with hyposmolar fluids during exertion (Severe symptomatic hyponatremia has been reported in marathon runners and in recreational hikers in the Grand Canyon.)

= 2[Na+ ] + [Glucose]/18 + [ BUN ]/2.8 = 2[123 mEq/L] + [98 mg/dL]/18 + [ 22 mg/dL ]/2.8 = = mOsm/Kg  NV = mOsm/Kg

= 2 [Na] + [Glucose]/18 = 2 [123] + [98]/18 = = mOsm/Kg NV = mOsm/Kg

 Osmolality of blood increases with dehydration  decreases with overhydration.  increased osmolality in the blood will stimulate secretion of antidiuretic hormone (ADH). This will result in increased water reabsorption, more concentrated urine, and less concentrated blood plasma.

 A low serum osmolality will suppress the release of ADH, resulting in decreased water reabsorption and more concentrated plasma.  changes in ECF osmolality have a great affect on ICF osmolality - changes that can cause problems with normal cell functioning and volume.

 Urine osmolality is a measure of urine concentrationin  large values indicate concentrated urine and small values indicate diluted urine.  important test for the concentrating ability of the kidney.  For determining the differential diagnosis of hyper- or hyponatraemia.

 For identifying SIADH (urine osmolality > 200 mmol/kg, urine sodium > 20 mmol/L, low serum sodium, patient not dehydrated and no renal, adrenal, thyroid, cardiac or liver disease or interfering drugs)  For identifying and diagnosing diabetes insipidus (low urine osmolality not responding to water restriction).

 For differentiating pre-renal from renal kidney failure (high urine osmolality is consistent with pre-renal impairment, in renal damage the urine osmolality is similar to plasma osmolality).

 The sodium urine test measures the amount of salt (sodium) in a urine sample.  Normal values are generally 15 to 250 milliequivalents per liter per day (mEq/L/day), depending on how much fluid and salt you consume.

 Greater than normal urine sodium levels may be caused by too much salt in the diet.  Lower than normal urine sodium levels may indicate:  Aldosteronism  Congestive heart failure  Diarrhea and fluid loss  Kidney failure

 Total Body Water (TBW)  Men ▪ TBW = 0.6 x weight  Women ▪ TBW = 0.5 x weight  Total Body Sodium Deficit  Sodium deficit = TBW x (140 - Serum Sodium)

Total Body Water (TBW) – Women TBW = 0.5 x weight = 0.5 X 50 kg = 25 Total Body Sodium Deficit – Sodium deficit = TBW x (140 - Serum Sodium) = 25 X (140meq/L-123meq/L) = 425

Total Body Water (TBW) – Women TBW = 0.5 x weight = 0.5 X 53 kg = 26.5 Total Body Sodium Deficit – Sodium deficit = TBW x (140 - Serum Sodium) = 26.5 X (140meq/L-123meq/L) = 450.5

 Two goals:  Raise plasma Na concentration by restricting water intake and promoting water loss  Correct underlying disease  Asymptomatic hyponatremia w/ECF vol contraction  Na + repletion w/ isotonic saline solution.

 Hyponatremia & edema  Restriction of Na + & water intake  Correction of hypokalemia  Promotion of water loss in excess of Na +

 Osmotic demyelination syndrome (central pontine myelinolysis )  Flaccid paralysis, dysarthria, dysphagia, and alterations of consciousness

 Asymptomatic patients:  Isotonic saline  Raised no more that 0.5 to 1.0 mmol/L per hour and by less than 10 to 12 mmol/L over 1 st 24 hr  Acute/severe patients:  Hypertonic saline  Raised by 1 to 2 mmol/L per hr for the 1 st 3 to 4 hr or until seizure subsides