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Consultant Emergency Department. Case 34 year old female, c/o weakness, nausea, dyspnea for several weeks, much worse past few days, no fever, occ vomiting,

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Presentation on theme: "Consultant Emergency Department. Case 34 year old female, c/o weakness, nausea, dyspnea for several weeks, much worse past few days, no fever, occ vomiting,"— Presentation transcript:

1 Consultant Emergency Department

2 Case 34 year old female, c/o weakness, nausea, dyspnea for several weeks, much worse past few days, no fever, occ vomiting, some abdominal discomfort, no cough. BP 80/40, HR 100, a febril, RR 24, diaphoretic Lungs occ. basilar crackle, abd soft, non tender, Card. regular, no murmer, no rub IV, O2, monitor….EKG


4 Empirically treated with Ca Gluconate with narrowing of QRS Stat K+ 8.6, previously healthy now with ARF, acidosis

5 Physiology, total body balance, and pathophysiology of potassium All disorders of potassium occur because of abnormal potassium handling in one of three ways: potassium intake, problems with distribution of potassium between the intracellular and extracellular spaces, or problems with potassium excretion

6 Clinical manifestations of hyperkalemia the organ systems affected are cardiac, neuromuscular, and gastrointestinal. Patients often complain of only vague feelings of not feeling well, gastrointestinal symptoms, or generalized weakness

7 Etiologies of hyperkalemia

8 Hyperkalemia = EKG


10 Emergency hyperkalemia = wide QRS

11 ECG changes

12 1. Tall peaked T waves(5.5-6.5) 2. P-R prolongation 3. Loss of p wave (6.5-7.5) 4. Widening of QRS (>8.0) 5. Sine Wave

13 Treatment of Hyperkalemia

14 Case 32 y/o F c/o several weeks of increasing muscle weakness, generalized. No N/V, no fever, no vision or speech problems, no other complaints, able to ambulate short distances with assist. PMH: neg Px: VSS, exam benign except strength 3/5 throughout, symmetric, CN intact Labs remarkable for K+ 1.9, total CK 1560

15 Hypokalemia Usually benign, worst complications 1) cardiacarrythmias, 2) rhabdomyolysis Most Common ED causes 1) Diuretics 2) Malnutrition, esp ETOH abuse 3) Vomiting +\- diarrhea (with vomiting due to renal losses as body tries to retain H+) Renal losses—diuretics (blocked reabsorption), steroid excess (aldosterone excess), Metabolic alkalosis (K lost in attempt to retain H+), Drugs (ampho, gent, ticarcillin) Endocrine—Cushing’s metabolic alkalosis syndrome (or steroid ingestion, DKA, Bartter’s Syndrome

16 Hypo K S&S and ECG changes Usually nonspecific—weakness, muscle pain, rhabdo EKG Changes of HypoK 1) Loss of T waves 2) U waves 3) Prolonged QT 4) Arrhythmias— Atrial—PSVT, afib Torsades, PVCs, VT, VF 5) NSST, T wave changes

17 Treatment of Hypo K


19 Hyponatremia Hyponatremia is defined as a serum sodium concentration less than 135 mEq/L. incidence of about 1% in the US population In acute and symptomatic cases, hyponatremia can result in significant mortality, with death rates as high as 17.9%

20 It is unclear whether the high mortality is caused by the hyponatremia itself, the underlying disease process, or the sequelae of overly aggressive hyponatremia management

21 Emergency department presentation The signs and symptoms of hypo natremia depend not only on the absolute serum sodium level, but also on the rate of serum sodium decline. Chronically hypo natremic individuals may be asymptomatic Acutely hypo natremic patients may be quite symptomatic with only mild hyponatremia


23 Emergency department presentation Sodium less than 125 mEq/L : Nausea, headache, myalgia, generalized malaise, and depressed deep tendon reflexes Sodium below 115 to 120 : Lethargy, confusion, disorientation, agitation, depression, psychosis, and eventually seizures, coma, and death

24 Classification

25 Emergency department evaluation Patients, especially high-risk patients, should be evaluated for hyponatremia in the ED if they exhibit nonspecific or neurological symptoms.

26 Risk factors include (1) Extremes of age (3) A history of malignancy (5) Recent surgical procedure (2) Diuretic, thiazide (4) Pulmonary or CNS disease (6) Psychiatric disease

27 The physical exam should focus not only on the neurological exam but also the determination of the patient’s clinical volume status The initial laboratory workup of a hyponatremic patient include determination of other serum electrolytes, renal function, plasma and urine osmolality, and urine sodium concentration

28 Emergency department management The two primary goals of ED therapy are to initiate the treatment of the underlying condition and to restore normal serum osmolality without causing an iatrogenic complication.

29 Classification

30 Fluid resuscitation rate Many ED patients initially receive an empiric 500 mL bolus of 0.9% normal saline (154 mEq/L sodium) before their laboratory results reveal a hyponatremic state

31 For documented hyponatremic patients with significant neurological symptoms, such as seizures, severe altered mental status, or coma, aggressive therapy is necessary to avoid permanent neurological deficits and even death from cerebral edema.

32 The high likelihood of cerebral edema outweighs the risk of possible ODS. In these patients, the target rate of correction is 1.5 to 2mEq/L per hour with 3% hypertonic saline for the first 3 to 4 hours, or more briefly, if symptoms improve The maximum rise of serum sodium concentration should not exceed 10 mEq/L in the first 24 hours


34 For hyponatremic patients with mild symptoms, the risk of ODS outweighs the risk of cerebral edema. These patients tend to have chronic (greater than 48 hours duration) hyponatremia. ODS very rarely develops if sodium correction is limited to 0.5 mEq/L per hour (approximately 500 Ml per hour of 0.9% saline in a 70 kg elderly male) with a maximum sodium increase of 10 to 12 mEq/L over 24 hours

35 Treatment complication : osmotic demyelination syndrome The rate of fluid resuscitation for hyponatremia is based on the patient’s symptomatology. The risks of hyponatremia-induced cerebral edema mustbe weighed against the therapeutic risk of developing osmotic demyelination syndrome (ODS)


37 Hypernatremia Hypernatremia is defined as a serum sodium concentration greater than 145 mEq/L. It is characterized by a deficit of TBW relative to total- body sodium

38 Always with total body water deficit in the adult Rare in awake people capable of drinking! Most common in elderly or infants, or people with AMS Symptoms usually when acute increases in Na to 158- 160 mEq/L Early s&s anorexia, weakness, N/V, later AMS, irritability, stupor, coma



41 Hypernatremia with volume loss and Low Total Body NA Heat stroke Diarrhea Osmotic diuresis—glucose, mannitol, enteral feedings RX: NS bolus until BP stable, then 1/2NS at 100cc/h until stable Goal to lower NA ~0.5meq/hr once total body water normalized

42 HyperNatremia with Low TBW and NormalTB Sodium Diabetes Insipidus Elderly with “reset” osmostat Hypothalamic dysfunction RX: ½ NS or encourage fluids per oral DDAVP for DI

43 Hypernatremia with Increased TB Sodium Usually iatrogenic—salt tablets, NS IVF, IV Na HCO3, feeding formula error Occasionally endocrine—Cushing’s or Conn’s syndrome RX: Water po, D5W or ½ NS and po fluids, dialysis if CRF Volume Depletion with hypotension ALWAYS requires NS fluid resuscitation regardless of serum sodium

44 Case 63 y/o M c/o abdominal pain, distention, nausea, ocasional vomiting, decreased appetite, several weeks of constipation, no BM for 10 days, had been to PMD with same complaints, OTC laxatives and enemas without relief PMH: hypertension Meds: SH: no drugs VS: HR 88 BP 154/90, RR 16, afeb Px: Abdomen: distended, obese, no peritoneal signs, lungs clear, ext without edema, neuro nonfocal Labs: Creat 1.8, Calcium 15.2, increased total protein and decreased albumin

45 Serum calcium 50% ionized, 40% protein bound, 10% chelated For hypercalcemia total calcium is adequate, for hypocalcemia ionized is more accurate,add 0.8mg/dl to serum calcium for every 1 gm/dl below 4 in hypoalbuminemia

46 Hypercalcemia Most Common Cause Malignancy-breast MC, lung, hematologic, kidney, prostate— direct bony destruction, ectopic PTH and PTH like substances Drugs—thiazides, calcium, estrogens, lithium, Vit A&D Hyperparathyroidism—primary and secondary Other Endocrine-MENs, hyperthyroidism, Pheochromocytoma, myxedema, adrenal insufficiency Iatrogenic Infections—AIDS, sarcoid, TB, granulomatous dz Renal disease —pseudo or secondary hyperPTH, tertiary if fails med rx, can lead to calciphylaxis Misc—dehydration, rhabdo, familial, idiopathic infantile

47 Symptoms and signs : Lethargy, AMS, Coma, Seizure, irritability Nausea,Vomiting, anorexia, constipation Abdominal Pain due to PUD, Pancreatitis, renal stones

48 EKG changes in Hypercalcemia shortened QT interval

49 ED Eval and Rx Mild elevations in asymptomatic patients may be sent for outpt eval, repeat fasting calcium, consider meds as cause Symptomatic patients—initial therapy NS bolus until BP and perfusion restored—inhibits prox reabsorption of Ca, continue 150-200cc/hr, monitoring cardiopulm status Lasix—inhibits distal reabsorption of Ca—only after tank is full! Follow Mag and K, replete K when urine output increased Renal Failure—dialysis, also in pulmonary edema

50 Other Medications Biphosphonates---inhibit osteoclast activity Steroids—inhibit vitamin D effect, decrease gut absorption of Ca, increased renal excretion, particularly in granulomatous dz Calcitonin—CRF, CHF, takes 8-24hrs,fails 25%, can cause allergic rxn Mithramycin—myeloma, takes 1-2 days

51 Hypocalcemia Sxs: perioral numbness, paresthesias, muscle cramps, irritability—progress to AMS, seizure, tetany, hypotension, acute heart failure, prolonged QT Chvosteks-tapping in front of ear causes facial muscle spasm, + 10-30% of normal calcium Trosseaus’s—tapping on median nerve or inflating BP cuff cause carpal spasm Hypocalcemia usually hypo magnesemai also RX oral or IV calcium


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