Consultant emergency medicine Security Forces Hospital Ministry of Interior KSA

Transcription

1 Consultant emergency medicine Security Forces Hospital Ministry of Interior KSA

2 Why Electrolytes are Important? IMMEDIATE LIFE THREAT. You can Save or KILL the patient fixing it. USEFUL CLUE to the UNDERLYING DIAGNOSIS.

3 Case 34 y/o F, 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, afeb, RR 24, diaph Lungs occ basilar crackle, abd soft, NT, card regular, no murmer, no rub IV, O2, monitor.ekg

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5 Empirically treated with calcium gluconate with narrowing of QRS Stat K+ 8.6, previously healthy now with ARF, acidosis

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

7 Clinical manifesta7ons 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

8 E7ologies of hyperkalemia

9 Hyperkalemia Pseudohyperkalemia Hemolysis of sample Distal to tourniquet Same IV potassium line Thrombocytosis > Leukocytosis > Laboratory error

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12 Hyperkalemia = EKG

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14 Emergency hyperkalemia = wide QRS

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16 ECG changes

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

18 Treatment of Hyperkalemia

19 35 y/o male c/o sudden onset of leg weakness x 4 hours now affecting one arm. Can not stand. No meds. PMHx Thyroid problem. No other sxs. Exam: 3/5 motor in (B) lower extremities and (L) upper extremity. Hyporeflexia throughout. Guillain- Barre, right?

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21 Potassium 1.9

22 Hypokalemia Usually benign, worst complications 1) cardiac arrythmias, 2) rhabdomyolysis MC 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), DKA (may present with elevated K due to extracellular shift), RTA, ETOH (diuretic) Endocrine Cushing s metabolic alkalosis syndrome (or steroid ingestion, DKA, Bartter s Syndrome

23 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) NS ST, T wave changes

24 Treatment of Hypo K

25 HYPOKALEMIA =HYPOMAGNESEMIA

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27 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% 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

28 Hyponatremia The signs and symptoms of hyponatremia depend not only on the absolute serum sodium level, but also on the rate of serum sodium decline. Chronically hyponatremic individuals may be asymptomatic Acutely hyponatremic patients may be quite symptomatic with only mild hyponatremia

29 Hyponatremia 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

30 Is the Hyponatremia Hypotonic, Isotonic or Hypertonic? Is it real Hypo- Na+? Hypertonic Hyponatremia: HONKS low Na+ is due to osmotic effects of other solutes: glucose actually dehydrate cells. Add 1.6 meq for each 100 mg/dl increase in Glucose. Isotonic Hyponatremia: (Pseudohyponatremias: Hypertriglyceridemia or paraproteinemias.) Hypotonic Hyponatremia: Most common scenario. Practically speaking: If they are not HONK or pseudohypernatremia, they are hypotonic and they are real Hypo- Na+. (Pt will have a low measured serum OsM.)

31 Volume Status Points to Dx anddirects Tx Hypovolemic: (Pediatric diarrhea, thiazide diuretics, blood loss.) Euvolemic: (SIADH, drugs, polydipsia) Hypervolemic: (CHF, Nephrotic syndrome, Cirrhosis, relative hypovolemia)

32 Hyponatremia The Role of ADH ADH sucks back FREE WATER at the collecting tubules and lowers Na+,. Trigger for ADH release is an increase in serum osmolality above 280. Hypovolemia (baroceptors) and other things: SIADH, Tegretol, etc. can lead to ADH release even when things are isotonic.

33 Causes of hyponatremia

34 Causes of SIADH

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37 Emergency department evalua7on Risk factors include 1. extremes of age; 2. recent initiation of a diuretic, especially a thiazide; 3. a history of malignancy; 4. pulmonary or CNS disease; 5. recent surgical procedure, 6. psychiatric disease

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39 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.

40 Is the Patient Symptomatic? (Szs/ AMS. Na+ usually <120) What is the VOLUME status? Symptomatic Euvolemic & Hypervolemic Patients Need Hypertonic Saline. Symptomatic Hypovolemic Patients Need volume expansion with Normal Saline

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42 Symptoma7c hyponatremia 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.

43 Symptoma7c hyponatremia The high likelihood of cerebral edema outweighs the risk of possible ODS. The target rate of correction is 1.5 to 2mEq/L per hour in case of acute hyponatremia, and 0.5meq/l in case of chronic 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 Na level should not be corrected above 120

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45 3% Hypertonic Saline Made Ridiculously Simple Use only if there are neurological sxs. Infuse at rate of: 1-2 ml/kg/hr, or roughly 100 ml/ hour for 4 hours. Check sodium every hour for first 4 hour. Stop infusion when Neuro Sxs resolve.

46 Hyponatremia asymptoma7c 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, with a maximum sodium increase of 10 to 12 meq/l over 24 hours

47 Treatment complica7on: osmotic demyelination syndrome The rate of fluid resuscitation for hyponatremia is based on the patient s symptomatology. The risks of hyponatremia- induced cerebral edema must be weighed against the therapeutic risk of developing osmotic demyelination syndrome (ODS)

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49 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 Always hypertonic. Always causes cellular dehydration. Rapid overcorrection of Na+ with hypotonic fluids can lead to cerebral edema due to the accumulation of idiogenic osmoles.

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51 Hyper natremia 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 meq/l Early sxs anorexia, weakness, N/V, later AMS, irritability, stupor, coma

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53 Hypernatremia with volume loss and Low Total Body NA Heatstroke 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

54 HyperNatremia with Low TBW and Normal TB Sodium Diabetes Insipidus Hypothalamic dysfunction RX: ½ NS or encourage fluids po DDAVP for DI

55 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 1/NS and po fluids, dialysis if CRF Volume Depletion with hypotension ALWAYS requires NS fluid resuscitation regardless of serum sodium

56 Thank you?

57 Case 63 y/o M c/o abd pain, distention, nausea, occ 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: HCTZ, SH: no drugs VS: HR 88 BP 154/90, RR 16, afeb Px: Abd: 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

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

59 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 dz pseudo or secondary hyperpth, tertiary if fails med rx, can lead to calciphylaxis Misc dehydration, rhabdo, familial, idiopathic infantile

60 S&S Lethargy, AMS, Coma, Sz, irritability N,V, anorexia, constipation Abd Pain due to PUD, Pancreatitis, renal stones

61 EKG changes in Hypercalcemia - - shortened QT interval

62 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 cc/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

63 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

64 Hypocalcemia Sxs: perioral numbness, paresthesias, muscle cramps, irritability progress to AMS, sz, tetany, hypotension, acute heart failure, prolonged QT Chvosteks- tapping in front of ear causes facial muscle spasm, % of normal calcium Trosseaus s tapping on median nerve or inflating BP cuff cause carpal spasm Hypocalcemia usually hypo mag also RX po or IV calcium