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«Fluids, Electrolytes and Acid/Base Balance PROBLEM 1 Severe Hypochloremic, Hypokalemic Metabolic Alkalosis with Intravascular Volume Deficit A 45 ...»

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PBL questions and answers

Fluids, Electrolytes and Acid/Base Balance


Severe Hypochloremic, Hypokalemic Metabolic Alkalosis with Intravascular Volume Deficit

A 45 year old man with previously known duodenal ulcer disease presents with complaints of persistent

vomiting for the past 36 hours. The vomit is clear-looking and acidic in taste. He has no abdominal pain.

Prior to the vomiting, he had difficulty with solid foods causing "fullness" in the stomach and he had been taking only liquids for one week. His heartburn had been aggravated at the time of the "fullness", but antacids did not help and he did not seek medical attention until today. He complains of being dizzy when he stands up. His blood pressure changes from 120/70 when lying to 105/55 when standing, his pulse changes from 100 to 130.

Study Questions:

1. What is the electrolyte composition of gastric contents?

Na+ 20-120 mEq/L; Cl- 130 mEq/L; K+ 10-15 mEq/L; HCO3- (-); H+ 30-100 mEq/L (KEY CONCEPT: high in Cl-, K+, H+; can rationalize the type oc acid-base disturbance observed based on this knowledge)

2. What is the most likely acid-base disturbance in the patient?

Metabolic alkalosis (see title)

3. What percentage of intravascular volume has been lost?

Orthostatic--can relate analogously to Class II type shock (15-30% volume loss)--can also see decreased pulse pressure Class I shock: typically see no physical exam changes.

Class III: (30-40%)-marked tachycardia, decreased systolic blood pressure, and oliguria Class IV: (40%)-significantly decreased systolic BP, severe oliguria/anuria; imminently life threatening

4. What intravenous fluid would be most likely to correct the acid/base and volume deficit?

0.9% NaCL (also replete K+ separately)--leads to decreased resorption and increased excretion of HCO3 – Na/HCO3 cotransporter in prox tubules (3:1 ratio) – therefore by replacing sodium with volume you decrease the HCO3 reabsorption here.

5. How much would be needed to replace the intravascular volume deficit?

TBW=60% (body Weight) TBW=2/3 Intracellular Volume (40%); 1/3 Extracellular Volume (20%) Extracellular Volume=3/4 Interstitial Fluid; ¼ Plasma Volume (4-5%) of TBW In 70 Kg man, the plasma volume is thus about 3 - 3.75 L. (appr. 2L RBC) A loss of blood volume of 30% corresponds to an approximate 1.5 L loss (assuming 5L blood volume): 14 L is the Extracellular Volume in a 70-kg person.

1.5 L x 14 L/3.75 L = 5.6 L OR Volume deficit = blood volume (66mL/kg males, 60mL/kg females) X %loss BV Resuscitation volume = VD x 4

6. What would be the sodium, potassium, and hydrogen ion concentration in the urine (normal, high, low for each)?

Na+ low, K+ high (aldosterone effects); H+ high (paradoxical aciduria)--this latter occurs as hypokalemia worsens and the kidneys try to preserve K+ in exchange for excreting H+. – draw aldosterone pathway PROBLEM 3 Excessive Ileostomy Output and Dehydration A 36 year old man has undergone a total colectomy and proctectomy for ulcerative colitis two years previously, and has an ileostomy which usually drains about 800 cc per day. Two days before coming to the hospital he developed crampy abdominal pain, bloating, and began draining large quantities of liquid from his ileostomy. Because of nausea and two episodes of vomiting he did not take any food or liquids over the past 24 hours.

Study Questions:

1. What is the usual amount of ileum output into the colon each day?

1-3 L

2. What are the electrolytes of ileostomy output?

New ostomy: Na+ 130, K+ 20, Cl- 110, HCo3 30 Adapted ileostomy: Na 50, K+ 5, Cl- 30, HCO3 25 LR – Na 130, Cl 109, lactate 28, 4mEq K, 3mEq Ca pH = 6.5, but is an alkalizing solution (because lactate is converted to bicarb)

3. What would be physical examination evidence of dehydration?

Dry mucous membranes, tachycardia, low urine output, decreased pulse pressure/systolic pressure (more extreme)

4. What laboratory tests would you order to assess the degree of dehydration and what alterations would you expect?

Panel 7 (increased BUN/Cr ratio) Urine electrolytes (FeNA)--1%

5. What intravenous fluid would you administer to replace the ileostomy output?

LR or D51/2 NS c 20 K PROBLEM 5 Measurement of Fluid Balance A 65 year old man with known congestive heart failure treated with digoxin and a diuretic undergoes an uneventful abdominal aortic aneurysm repair with 1,000 cc of blood loss. During the four hours of surgery he is administered 4,000 cc of lactated Ringer's solution. During his first eight hours after surgery he is administered 1,000 cc of lactated Ringer's, has made 250 cc of urine and has drained 200 cc from a nasogastric tube.

Study Questions:

1. What methods would you use to evaluate the intravascular volume status in this patient eight hours after surgery?

Urine output, CVP, SG catheter, Urine electrolytes (FENA), physical exam findings-edema etc.

2. What methods would you use to evaluate the total body fluid status of this patient?

Physical exam-edema, total body weight, Serum Na PROBLEM 8 Hyponatremia A 55 year old woman with alcoholic cirrhosis and ascites is admitted for upper intestinal bleeding.

Upper endoscopy reveals gastritis which is not actively bleeding. She is admitted and given an intravenous of 5% dextrose and 0.2% NaCl at 125 cc/hr. Over the next 24 hours her abdomen becomes tense and her urine output is 15 to 20 cc per hour. Her serum sodium has decreased from 132 on admission to 122 and she is less responsive to verbal stimuli.

Study Questions:

1. What are possible etiologies of hyponatremia?

Pseudohyponatremia (protein, lipids) Dilutional hyponatremia (hyperglycemia, mannitol) True Hyponatremia-Decreased ECF volume: (plasma, GI skin, renal losses) Nl ECF volume: (SiADH, psychogenic, hypothyroidism, hypoadrenalism) Expanded ECF volume: CHF, cirrhosis, nephritic syndrome, malnutrition

2.What is the most likely etiology in this patient?

Cirrhosis (expanded ECF volume)

3. What happens to urine sodium concentrations with the several etiologies listed above?

Psychogenic (100) SiADH (100) Heart Failure (Low Urine Na+) Renal Failure (High Urine Na+)

4.What is the treatment of hyponatremia in this patient?

Free water restrict; + Na restrict (loop diuretic) PROBLEM 12 Acute Renal Failure A 64 year old man has surgical resection of an abdominal aortic aneurysm with graft interposition. The operation is difficult and six units of packed cells are infused during the surgery. The patient's blood pressure twice fell to 70 systolic during the four-hour operation. Eight liters of crystalloid were administered, 500 cc of fresh frozen plasma, and 1,000 cc of Hetastarch. The patient came to the intensive care unit with a systolic blood pressure of 60 mmHG. Three additional units of blood were given before his pressure is over 100 mmHg systolic. The patient made 100 cc of urine output during the case but in the ICU is noted to be oliguric, with 5 to 10 cc of urine output during the first four postoperative hours. Mannitol, which was given in the operating room, was repeated with no increase in urine output. During the next twelve hours six liters of crystalloid and 500 cc of packed red cells are administered resulting in 75 cc of dark yellow urine. By this time his hemoglobin and hematocrit have stabilized at 9.6 gms and 27.8%.

–  –  –

1.What is the differential diagnosis of the oliguria? The most likely diagnosis?

Pre-renal; Intra-renal; Post-renal

2. What is the most likely etiology?


3. What is the natural history of this disease?

The disease typically lasts 1-3 weeks as tubular cells regenerate after ischemic insult, but course may be quite variable depending upon extent of initial insult.

4. What are the principles of management of this disease IV hydration Cease nephrotoxic drugs Optimize oxygen delivery to organ systems Potentially Dialysis (Sometimes diuretics are used to maintain urine output in the setting of renal failure, but studies have not shown a benefit to ultimate kidney(s) or patient survival with this approach.

Biliary Tract


Gallstones A 19 year old woman presents with history of intermittent epigastric and right upper quadrant pain which occurs about 15 minutes after eating and lasts for one to two hours. This pain has been happening for about one month, two to three times a week, especially after eating french fries. She is 5 ft. 4 inches tall and weighs 130 pounds. She has never been pregnant and is currently taking birth control pills. Physical examination is normal. An ultrasound of the gallbladder demonstrates multiple small stones.

Background info:

Approximately 8% males and 17-20% females have gallstones 80% of those are asymptomatic and 20% are symptomatic 2% of the asymptomatic patients will become symptomatic 75% of those have bilary colic. 30% of pts with biliary colic develop acute cholecystitis.

Bile contains bile salts, phospholipids (in the form of lecithin), and cholesterol. Any imbalance of the three will cause lithogenic bile. Excess cholesterol relative to the bile salts and lecithin will cause gallstone formation.

DDX of RUQ pain: PUD, pancreatitis, appendicitis, RLL PNA, cecal volvulus, MI, hepatic congestion, FitzHugh-Curtis, hepatitis, Mirizzi syndrome.

Study Questions:

1. What types of gallstones can be formed? Which type is most likely in this patient?

3 Types of gallstones:

Mixed (80%- most common type): approx 70% cholesterol Pure Cholesterol (10%): often solitary, large, non-calcified Pigment (10%): composed of unconjugated bilirubin, calcium, and organic material. Black stones associated with cirrhosis and chronic hemolytic states. Usually sterile. Brown stones are associated with biliary stasis and more frequently found in CBD. Usually infected.

2. What factors predispose to the formation of gallstones?

Elevated estrogen and progesterone levels (fertile female/pregnant females), older age, DM, obesity, IBD, starvation/NPO, TPN, hemolytic states, rapid weight loss, malabsorptive states, certain race/ethnic backgrounds.

3. What is the pathophysiology of chronic and acute cholecystitis? What are the presenting symptoms, physical examination, and laboratory findings for each? Which one does this patient have?

95% of acute cholecystitis cases are due to obstruction of cystic duct by stones, which leads to bilary stasis and bacterial overgrowth and infected bile. The difference between acute and chronic cholecystitis is that acute is severe enough to cause patients to seek medical attention right away whereas chronic patients develop either multiple mild acute symptoms or smoldering infections for long periods.

Sx: RUQ pain, N/V, fever, anorexia Signs: mod elevation of WBC, alk phosphatase, and possible elevation of LFTs, temp, murphy’s sign, peritonitis/sepsis, palpable gallbladder.

4. What are the treatment options for chronic and acute cholecystitis?

Admit, NPO/IVF, IV abx, Lap vs open cholecystectomy 24-48hrs upon admission. Perc. cholecystostomy tube for unstable or patients that would not tolerate an operation.

5. What complications of gallstones might develop in this young female if the gallbladder is not removed?

Hydrops, gangrene or perforation of gallbladder, suppurative cholecystitis, cholecystenteric fistula, gallstone ileus, sepsis, death. Most common microbes: E. Coli, Klebsiella, enterococcus, enterobacter PROBLEM 51 Choledocholithiasis A 36 year old woman presents to the emergency room with a history of right upper quadrant pain, shaking chills, and jaundice. This pain came on suddenly six hours earlier and has been progressing. She took her temperature at home and it was 102. She vomited once at the onset of the pain. She has had intermittent episodes of epigastric and right upper quadrant pain after eating for the past six months.

The pain always abated after thirty to sixty minutes. Her blood pressure is 110/60, her pulse 110, and her temperature 39 in the emergency room.

Background info:

Approx. 8-16% of pts w/ stones will have stones found in the CBD.

Most arise from the gallbladder thus secondary CBD stones Stones that form de novo in the CBD are referred to as primary stones and almost always associated with bile stasis.

Study Questions:

1.How is extra-hepatic obstructive jaundice differentiated from other etiologies?

Lab values, radiographs (U/S, CT, ERCP/MRCP)

2. What are the etiologies of obstructive jaundice?

Stone, stricture, cancer (head of pancreas/bile ducts) or intrinsic or extrinsic tumors, primary sclerosing cholangitis, acute and chronic cholangitis, parasitic infections (liver flukes or ascaris lumbricoides), choledochal cysts, and AIDS cholangiopathy.

3. What tests would you use to differentiate etiologies of obstructive jaundice?

Lab values (elevated T. bili., D-bili., GGT, AP, AST/ALT [normal in early stage] + urine bilirubin), Signs (clay-colored stools, dark urine, jaundice [90%], scleral icterus, hepatomegaly[20-40%], RUQ mass), Sxs (pruritis [66%], abd pain[30-50%], wt loss[30-50%], fever[20%]). Courvoisier’s sign (palpable gallbladder) RUQ U/S: best to evaluate bile ducts ERCP/MRCP: diagnostic and therapeutic CT of abdomen/pelvis PTC +/- Bx

4. Which etiology is most likely in this case? What are the treatment priorities and management options for this case?

Pt’s w/ Charcots triad (RUQ pain, fever, jaundice) or Reynolds pentad (charcot + hypotension/MS change) is an emergency and rapid decompression of the biliary tree is necessary. O/W make pt NPO/IVF, IV abx, ERCP/sphincterotomy and stone retrieval, then urgent lap vs open cholecystectomy +/IOC (intraoperative cholangiography). If no ERCP, or if it is unsuccessful, then open surgical stone extraction with T-tube placement or choledocho-enterostomy.

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