This question is not an easy one. The available literature is somewhat controversial (some guidelines advise using glucose saline, others absolutely forbid it...) so I have decided to rely on the treatment recommended by Harrison, which is the manual that MIR examiners usually rely on. This girl presents with hypernatremia due to extrarenal free water losses. The goal is to replace the lost water and reduce the natremia at a rate of no more than 12 mmol/day. To calculate fluid therapy, the water deficit must first be calculated. Water def. Water = (Natremia-140/140)xTotal body water. TBW = Weight in kg x 0.4 in females/0.5 in males. In this case, the water deficit is: ([[tel:155-140/140|155-140/140]])x60x0.4 = 2.57 liters. There are only two answers that come close to this figure, but 2 seems more correct, as it is the only one that completely covers the water deficit and uses a hyposodium solution.

This question is not an easy one. The available literature is somewhat controversial (some guidelines advise using glucose saline, others absolutely forbid it...) so I have decided to rely on the treatment recommended by Harrison, which is the manual that MIR examiners usually rely on. This girl presents with hypernatremia due to extrarenal free water losses. The goal is to replace the lost water and reduce the natremia at a rate of no more than 12 mmol/day. To calculate fluid therapy, the water deficit must first be calculated. Water def. Water = (Natremia-140/140)xTotal body water. TBW = Weight in kg x 0.4 in females/0.5 in males. In this case, the water deficit is: ([[tel:155-140/140|155-140/140]])x60x0.4 = 2.57 liters. There are only two answers that come close to this figure, but [HIDDEN], as it is the only one that completely covers the water deficit and uses a hyposodium solution.

19-year-old woman, weight 60 kg, with acute dehydration due to long exposure to the sun. Blood pressure lying down 100/60 mmHg. Standing 70/50 mmHg with dizziness. Serum sodium levels 155 mmol/L. What is the most correct treatment, in the first 24 hours, taking into account the data available to us?

Hypertonic saline (3%), 500 ml + 500 ml of 5% glucose.

Hyperosmolar hyperglycemic state

Management Intravenous fluids Treatment of HHS begins with reestablishing tissue perfusion using intravenous fluids. People with HHS can be dehydrated by 8 to 12 liters. Attempts to correct this usually take place over 24 hours with initial rates of normal saline often in the range of 1 L/h for the first few hours or until the condition stabilizes. Electrolyte replacement Potassium replacement is often required as the metabolic problems are corrected. It is generally replaced at a rate 10 mEq per hour as long as there is adequate urinary output. Insulin Insulin is given to reduce blood glucose concentration; however, as it also causes the movement of potassium into cells, serum potassium levels must be sufficiently high or dangerously low blood potassium levels may result. Once potassium levels have been verified to be greater than 3.3 mEq/l, then an insulin infusion of 0.1 units/kg/hr is started. The goal for resolution is a blood glucose of less than 200 mg/dL. References

Gastric distension attenuates the hypotensive effect of intraduodenal glucose in healthy older subjects.

Postprandial hypotension occurs frequently, and current management is suboptimal. Recent studies suggest that the magnitude of the fall in postprandial blood pressure (BP) may be attenuated by gastric distension. The aim of this study was to determine the effect of gastric distension on the hypotensive response to intraduodenal (ID) glucose. Eight healthy subjects (5 males, 3 females, aged 65-76 years) received an ID infusion of either 1) 50 g glucose in 300 ml saline (ID glucose) over 60 min (t=0-60 min), 2) 50 g glucose in 300 ml saline over 60 min and intragastric (4) infusion of 500 ml water between t=7-10 min (IG water and ID glucose), or 3) ID saline (0.9%) infusion over 60 min and IG infusion of 500 ml water (IG water and ID saline) all followed by ID saline infusion for another 60 min (t=60-120 min) on three separate days. BP and heart rate (HR) were measured. Gastric emptying (GE) of the IG water was quantified by two-dimensional ultrasonography. Between t=0-60 min, systolic and diastolic BP was greater (P<0.05 for both) with IG water and ID saline compared with IG water and ID glucose, and less (P<0.05 for both) with ID glucose compared with IG water and ID glucose. These effects were evident at relatively low IG volumes (approximately 300 ml). GE was faster with IG water and ID saline when compared with IG water and ID glucose. We conclude that, in healthy older subjects, IG administration of water markedly attenuates the hypotensive response to ID glucose, presumably as a result of gastric distension.

The effect of an oral glucose load on sodium and water excretion after rapid intravenous infusion of 0.9% (w/v) saline.

Previous studies have suggested that oral or intravenous glucose enhances salt and water retention following a saline load. To test this, we studied the effects of an oral glucose load on urinary sodium and water excretion and serum biochemistry in response to a 2l intravenous infusion of 0.9% saline in normal subjects. A crossover study was conducted on six male volunteers. On one occasion, they received 2l 0.9% saline intravenously over 1h. A week later, they were given 100ml 50% dextrose orally prior to the same infusion. Subjects passed urine before start of the infusion. Body weight, haematocrit and serum biochemistry were recorded preinfusion and hourly for 6h. Urine was collected for 6h postinfusion and analysed for sodium, potassium and osmolality. The six subjects had a mean (SE) age of 20.9 (0.4) years and BMI of 22.7 (0.2). Median (IQR) water balance over 6h was 1462 (1005-1650)ml after saline and 1203 (989-1735)ml after glucose and saline (NS). Urinary sodium and potassium excretion on the two occasions over 6h were 76 (69-111) vs 74 (92-174)mmol and 31 (29-40) vs 30 (20-36)mmol, respectively (NS). Using repeated measures testing, there was no significant difference in body weight, haematocrit, serum albumin, sodium, potassium, chloride, osmolality and blood glucose measured at hourly intervals on the two occasions. In contrast to previous literature, in normal subjects, an additional oral glucose load does not appear to have an effect on urinary sodium excretion or serum biochemistry after a rapid 2l infusion of 0.9% saline. This does not preclude an effect under conditions of prior starvation or injury.

Hyponatremia

Total body water = kilograms of body weight x 0.6 Fluids Options include: Mild and asymptomatic hyponatremia is treated with adequate solute intake (including salt and protein) and fluid restriction starting at 500 millilitres per day (mL/d) of water with adjustments based on serum sodium levels. Long-term fluid restriction of 1,200–1,800 mL/d may maintain the person in a symptom-free state. Moderate and/or symptomatic hyponatremia is treated by raising the serum sodium level by 0.5 to 1 mmol per liter per hour for a total of 8 mmol per liter during the first day with the use of furosemide and replacing sodium and potassium losses with 0.9% saline. Severe hyponatremia or severe symptoms (confusion, convulsions, or coma): consider hypertonic saline (3%) 1–2 mL/kg IV in 3–4 h. Hypertonic saline may lead to a rapid dilute diuresis and fall in the serum sodium. It should not be used in those with an expanded extracellular fluid volume.

Intravenous sugar solution

Concentrated dextrose solutions should not be administered subcutaneously or intramuscularly as they can cause cell death via dehydration and subsequent necrosis. Types Types of glucose/dextrose include: D5W (5% dextrose in water), which consists of 278 mmol/L dextrose D5NS (5% dextrose in normal saline), which, in addition, contains normal saline (0.9% w/v of NaCl). D5 1/2NS 5% dextrose in half amount of normal saline (0.45% w/v of NaCl). D5LR (5% dextrose in lactated Ringer solution) D50 – 50% dextrose in water The percentage is a mass percentage (or more precisely, a mass-volume percentage), so a 5% glucose/dextrose solution contains 50 g/L of glucose/dextrose (5g/100ml). Glucose provides energy 4 kcal/gram, so a 5% glucose solution provides 0.2 kcal/ml. If prepared from dextrose monohydrate, which provides 3.4 kcal/gram, a 5% solution provides 0.17 kcal/ml. References External links

Crush syndrome

Intravenous hydration of up to 1.5 L/h should continue to prevent hypotension. A urinary output of at least 300 mL/h should be maintained with IV fluids and mannitol, and hemodialysis considered if an increase in urine is not achieved. Use intravenous sodium bicarbonate to keep the urine pH at 6.5 or greater, to prevent myoglobin and uric acid deposition in kidneys. To prevent hyperkalemia/hypocalcemia, consider the following adult doses: calcium gluconate 10% 10 mL or calcium chloride 10% 5 mL IV over 2 minutes sodium bicarbonate 1 meq/kg IV slow push regular insulin 5–10 U 50% glucose 1–2 ampules IV bolus kayexalate 25–50 g with sorbitol 20% 100 mL by mouth or rectum. Even so, abnormal heart rhythms may develop; electrocardiographic monitoring is advised, and specific treatment begun promptly. References External links Life or Limb: What happens when your leg gets trapped under a building? Injuries Early complications of trauma Nephrology Syndromes

InternalMed_Harrison

Fluid replacement should initially stabilize the hemodynamic status of the patient (1–3 L of 0.9% normal saline over the first 2–3 h). Because the fluid deficit in HHS is accumulated over a period of days to weeks, the rapidity of reversal of the hyperosmolar state must balance the need for free water repletion with the risk that too rapid a reversal may worsen neurologic function. If the serum sodium is >150 mmol/L (150 meq/L), 0.45% saline should be used. After hemodynamic stability is achieved, the IV fluid administration is directed at reversing the free water deficit using hypotonic fluids (0.45% saline initially, then 5% dextrose in water [D5W]). The calculated free water deficit (which averages 9–10 L) should be reversed over the next 1–2 days (infusion rates of 200–300 mL/h of hypotonic solution). Potassium repletion is usually necessary and should be dictated by repeated measurements of the serum potassium. In patients taking diuretics, the potassium deficit can be quite

Normal Saline -- Administration

Normal saline solution can be administered only via intravenous access. [2] When deciding dosage, the provider must take into account various patient factors (e.g., weight, age, clinical presentation, laboratory findings). Therefore, monitoring should focus on laboratory results and clinical evaluation (see ‘Monitoring’ section). Naturally, there are two methods of administration for normal saline: 1) Fluid bolus This route is normally used in the acute care setting when a rapid infusion of fluids is necessary (e.g., hypovolemia). Delivery of fluid should be administered through large-bore peripheral lines or via central-line access. [3] 2) Maintenance The calculation of daily fluid requirements is achievable in various ways. Common practices utilize the formulas created by Drs. Holliday and Segar which indicate that one can use the "100-50-25" or "4-2-1" rules. [4] Examples: For a 50 kg patient First 10 kg weight = 1000 mL (100 mL/kg x 10) Second 10 kg weight = 500 mL (50 mL/kg x 10)

Saline (medicine)

Normal saline (NSS, NS or N/S) is the commonly used phrase for a solution of 0.90% w/v of NaCl, 308 mOsm/L or 9.0 g per liter. Less commonly, this solution is referred to as physiological saline or isotonic saline (because it is approximately isotonic to blood serum, which makes it a physiologically normal solution). Although neither of those names is technically accurate because normal saline is not exactly like blood serum, they convey the practical effect usually seen: good fluid balance with minimal hypotonicity or hypertonicity. NS is used frequently in intravenous drips (IVs) for people who cannot take fluids orally and have developed or are in danger of developing dehydration or hypovolemia. NS is also used for aseptic purpose. NS is typically the first fluid used when hypovolemia is severe enough to threaten the adequacy of blood circulation, and has long been believed to be the safest fluid to give quickly in large volumes. However, it is now known that rapid infusion of NS

Saline (medicine)

The solution is 9 grams of sodium chloride (NaCl) dissolved in water, to a total volume of 1000 ml (weight per unit volume). The mass of 1 millilitre of normal saline is 1.0046 grams at 22 °C. The molecular weight of sodium chloride is approximately 58.4 grams per mole, so 58.4 grams of sodium chloride equals 1 mole. Since normal saline contains 9 grams of NaCl, the concentration is 9 grams per litre divided by 58.4 grams per mole, or 0.154 mole per litre. Since NaCl dissociates into two ions – sodium and chloride – 1 molar NaCl is 2 osmolar. Thus, NS contains 154 mEq/L of Na+ and the same amount of Cl−. This points to an osmolarity of 154 + 154 = 308, which is higher (i.e. more solute per litre) than that of blood (approximately 285). However, if the osmotic coefficient (a correction for non-ideal solutions) is taken into account, then the saline solution is much closer to isotonic. The osmotic coefficient of NaCl is about 0.93, which yields an osmolarity of 0.154 × 1000 × 2 × 0.93 =

Diabetic ketoacidosis

Fluid replacement The amount of fluid replaced depends on the estimated degree of dehydration. If dehydration is so severe as to cause shock (severely decreased blood pressure with insufficient blood supply to the body's organs), or a depressed level of consciousness, rapid infusion of saline (1 liter for adults, 10 ml/kg in repeated doses for children) is recommended to restore circulating volume. Slower rehydration based on calculated water and sodium shortage may be possible if the dehydration is moderate, and again saline is the recommended fluid. Very mild ketoacidosis with no associated vomiting and mild dehydration may be treated with oral rehydration and subcutaneous rather than intravenous insulin under observation for signs of deterioration. Normal saline (0.9% saline) has generally been the fluid of choice. There have been a few small trials looking at balanced fluids with few differences.

InternalMed_Harrison

3. Assess: Serum electrolytes (K+, Na+, Mg2+, Cl−, bicarbonate, phosphate) Acid-base status—pH, HCO3−, PCO2, β-hydroxybutyrate Renal function (creatinine, urine output) 4. Replace fluids: 2–3 L of 0.9% saline over first 1–3 h (10–20 mL/kg per hour); subsequently, 0.45% saline at 250–500 mL/h; change to 5% glucose and 0.45% saline at 150–250 mL/h when plasma glucose reaches 250 mg/dL (13.9 mmol/L). 5. Administer short-acting insulin: IV (0.1 units/kg), then 0.1 units/kg per hour by continuous IV infusion; increase twoto threefold if no response by 2–4 h. If the initial serum potassium is <3.3 mmol/L (3.3 meq/L), do not administer insulin until the potassium is corrected. 6. Assess patient: What precipitated the episode (noncompliance, infection, trauma, pregnancy, infarction, cocaine)? Initiate appropriate workup for precipitating event (cultures, CXR, ECG). 7.

InternalMed_Harrison

Moderatec,d <4 months (<5 kg) 200–400 mL of ORS 4–11 months (5–<8 kg) 400–600 mL of ORS 12–23 months (8–<11 kg) 600–800 mL of ORS 2–4 years (11–<16 kg) 800–1200 mL of ORS 5–14 years (16–<30 kg) 1200–2200 mL of ORS ≥15 years (≥30 kg) 2200–4000 mL of ORS All ages and weights Undertake IV fluid replacement with Ringer’s lactate (or, if not available, normal saline). Give 100 mL/kg in the first 3-h period (or the first 6-h period for children <12 months old); start rapidly, then slow down. Give a total of 200 mL/ kg in the first 24 h. Continue until the patient is awake, can ingest ORS, and no longer has a weak pulse. aAdapted from World Health Organization: First steps for managing an outbreak of acute diarrhoea. Global Task Force on Cholera Control, 2009 (www.who.int/topics/cholera). bContinue normal feeding during treatment. cReassess regularly; monitor stool and vomit output. dVolumes of ORS listed should be given within the first 4 h. Abbreviation: ORS, oral rehydration solution.

[Anesthesia for cesarean section in a patient with transient diabetes insipidus].

A 32-year-old pregnant female was admitted to our hospital at 32 week gestation and was scheduled for emergent cesarean section because of fetal distress. She had been suffering hydrodipsia and dry mouth, and had lost 4 kg in 2 weeks. Hypernatremia, hyperchloremia, and lower urinary specific gravity were preoperatively noted. Her electrolyte imbalance was partially corrected by the infusion of 1400 ml of 5% glucose solution and 500 ml of acetated Ringer's solution, but unexpected hyperglycemia; 440 mg.dl-1, appeared before surgery. Cesarean section was successfully performed with spinal anesthesia. A 1566 g male infant was delivered with 1 and 5 min Apgar scores of 2 and 1. Hyperglycemia and secondary hypoglycemia occurred in the infant in the neonatal ICU. The mother's fluid loss, including blood and amniotic fluid, was estimated at 784 ml. Five hundred milliliters of acetated Ringer's solution and 1000 ml of half saline solution with 2.5% glucose were infused before delivery, followed by the glucose solution containing a low concentration of sodium after delivery. After surgery, high serum osmotic pressure and paradoxically low urinary osmotic pressure were found. The plasma antidiuretic hormone level was normal against the high serum osmotic pressure. The electrolyte imbalance and urinary osmotic pressure were improved by using I-deamino-8-d-arginine vasopressin, and DI was finally diagnosed. Hormonal therapy was discontinued on day 20, and the patient was discharged on day 21. Some pregnancies are complicated by transient DI. Anesthesiologists have to consider DI when a pregnant female has symptoms of dehydration and a significant electrolyte imbalance.

Effects of high-dose furosemide and small-volume hypertonic saline solution infusion in comparison with a high dose of furosemide as bolus in refractory congestive heart failure: long-term effects.

Diuretics have been accepted as first-line treatment in refractory congestive heart failure (CHF), but a lack of response to them is a frequent event. A randomized, single-blind study was performed to evaluate the effects of the combination of high-dose furosemide and small-volume hypertonic saline solution (HSS) infusion in the treatment of refractory New York Heart Association (NYHA) class IV CHF and a normosodic diet during follow-up. Materials and Methods One hundred seven patients (39 women and 68 men, age range 65-90 years) with refractory CHF (NYHA class IV) of different etiologies, who were unresponsive to high oral doses of furosemide, angiotensin-converting enzyme inhibitors, digitalis, and nitrates, were enrolled. Inclusion criteria included an ejection fraction (EF) <35%, serum creatinine level <2 mg/dL, blood urea nitrogen level < or =60 mg/dL, reduced urinary volume, and low natriuresis. The patients were randomized in 2 groups (single-blind). Patients in group 1 (20 women and 33 men) received an intravenous (IV) infusion of furosemide (500-1000 mg) plus HSS (150 mL of 1.4%-4.6% NACl) twice a day in 30 minutes. Patients in group 2 (19 women and 35 men) received an IV bolus of furosemide (500-1000 mg) twice a day, without HSS, during a period lasting 6 to 12 days. Both groups received IV KCl (20-40 mEq) to prevent hypokalemia. At study entry, all patients underwent a physical examination and measurement of body weight (BW), blood pressure (BP), and heart rate (HR), an evaluation of signs of CHF, and measurement of control levels of serum Na, K, Cl, bicarbonate, albumin, uric acid, creatinine, urea, and glycemia daily during hospitalization, and measurements of the daily output of urine for Na, K, and Cl. A chest radiograph, electrocardiogram, and echocardiogram were obtained at study entry, during hospitalization, and at the time of discharge from the hospital. During the treatment and after discharge, the daily dietary Na intake was 120 mmol in group 1 versus 80 mmol in group 2, with a fluid intake of 1000 mL daily in both groups. An assessment of BW and 24-hour urinary volume, serum, and urinary laboratory parameters were performed daily until patients reached a compensated state, when IV furosemide was replaced with oral administration (250-500 mg/d). After discharge from the hospital, patients were observed as outpatients weekly for the first 3 months and, subsequently, once a month. The groups were similar in age, sex, EF, risk factors, treatment, and etiology of CHF. All patients showed a clinical improvement. Ten patients in both groups had hyponatremia at entry. A significant increase in daily diuresis and natriuresis was observed in both groups, but it was more significant in the group receiving HSS (P <.05). The serum Na level increased in group 1 and decreased in group 2 (P <.05). The serum K level was decreased in both groups (P <.05). BW was reduced in both groups (P <.05). Group 2 had an increase in serum creatinine level. Serum uric acid levels increased in both groups. BP values decreased and HR was corrected to normal values in both groups. In the follow-up period (31 +/- 14 months), 25 patients from group 1 were readmitted to the hospital for heart failure. In group 2, 43 patients were readmitted to the hospital at a higher class than at discharge. Twenty-four patients in group 1 died during follow-up, versus 47 patients in group 2 (P <.001). This treatment is effective and well tolerated, improves the quality of life through the relief of signs and symptoms of congestion, and may delay more aggressive treatments. The effects were also beneficial in a long period for mortality reduction (55% vs 13% survival rate) and for clinical improvement.

Evaluation of an oral rehydration solution with Na+ 60 mmol/l in infants hospitalized for acute diarrhoea or treated as outpatients.

An oral rehydration solution (ORS) containing 60 mmol/l of Na+ (ORS60) was compared in a randomized trial with the ORS of WHO formula (Na+ 90 mmol/l = ORS90) for the treatment of diarrhoeal dehydration in 66 hospitalized infants aged 3 to 34 months. The infants had a 5 +/- 3% dehydration, and received within 6-10 hours 76 +/- 32 ml/kg of ORS60 or 74 +/- 41 ml/kg of ORS90 corresponding to a sodium input of 4.6 +/- 1.9 mmol/kg and 6.6 +/- 3.7 mmol/kg, respectively. Both treatments were found adequate and equally effective for the correction of dehydration and sodium deficit. The same ORS60 was also compared to a commercial low sodium glucose-electrolyte solution (sodium 35 mmol/l, glucose 3.5 milligrams) for ambulatory treatment of acute diarrhoea in infants. Satisfactory rehydration was achieved within 6 hours in 19 of 23 infants receiving ORS60 as opposed to 6 of 18 infants receiving the commercial solution (p less than 0.001); the poor result with the latter was in most cases attributed to a refusal by the infant to consume the sweetish solution. It is concluded that ORS60 is suitable for the treatment of isotonic diarrhoeal dehydration in hospitalized children as well as outpatients.

Hypertonic saline.

A key feature in the successful resuscitation of dehydrated or endotoxemic ruminants is the total amount of sodium administered. Administration of small volumes of HS and HSD offer major advantages over large volumes of isotonic saline because HS and HSD do not require intravenous catheterization or periodic monitoring, and are therefore suitable for use in the field. Hypertonic saline and HSD exert their beneficial effect by rapidly increasing preload and transiently decreasing afterload. Contrary to early reports, HS and HSD decrease cardiac contractility and do not activate a pulmonary reflex. The osmolality of HS and HSD should be 2400 mOsm/L (7.2% NaCl solution, 8 times normal plasma osmolality). Use of HS and HSD solutions of different osmolality to 2400 mOsm/L should be avoided at all costs, as too low a tonicity removes the main advantages of HS (low cost, decreased infusion time), whereas too high a tonicity may cause rapid vasodilation and decreased cardiac contractility, resulting in death. Rapid administration (> 1 mL/kg-1/min-1) of HS (2400 mOsm/L) should be avoided, as the induced hypotension may be fatal when coupled with a transient decrease in cardiac contractility. For treating dehydrated adult ruminants, HS (2400 mOsm/L, 4-5 mL/kg i.v. over 4-5 minutes) should be administered through the jugular vein and the cow allowed to drink water. This means that 2 L of HS should be administered to adult cattle. HSD should be administered in conjunction with isotonic oral electrolyte solutions to all calves 8% or more dehydrated (eyes recessed > or = 4 mm into the orbit, cervical skin tent duration > 6 seconds) or calves with reduced cardiac output (fetlock temperature < 29 degrees C when housed at 10-24 degrees C). For treating dehydrated calves, HSD (2400 mOsm/L NaCl in 6% dextran-70, 4-5 mL/kg i.v. over 4-5 minutes) should be administered through the jugular vein and the calf allowed to suckle an isotonic oral electrolyte solution. This means that 120-200 mL of HSD of HSD should be administered to a calf. HSD should be routinely administered to severely depressed or comatose calves, as HSD provides the fastest method of resuscitation while rapidly reversing the effects of hyperkalemia.

Cerebral Contusion -- Treatment / Management

If using a parenchymal ICP device, change to an EVD. Hyperosmolar therapy (mannitol or hypertonic saline), given intermittently. Mannitol administered in intermittent boluses (0.25 to 1 gm/ kg body weight). Check frequently the serum sodium and osmolality; additional doses held if serum osmolality exceeds 320 mOsm/L. Hypertonic saline 3% sodium chloride solution administered in intermittent boluses of 250 ml over 0.5 hours (2-5 mL/kg over 10-20 minutes). Serum sodium and osmolality checked every 6 hours. Additional doses held if serum sodium exceeds 160 mEq/L. A bolus of up to 23.4% sodium chloride solution can be given for refractory increased ICP. CPP no less than 50 mm Hg. (Goal between 60 and 70 mm Hg). PaCO2 goal of 30 to 35 mmHg should be maintained. Repeat head CT imaging if no improvement. Neuromuscular paralysis bolus test dose. If ICP remains ≥ 20 to 25 mmHg, proceed to Tier 3. Tier 3

Effects of high-dose furosemide and small-volume hypertonic saline solution infusion in comparison with a high dose of furosemide as a bolus, in refractory congestive heart failure.

Diuretics, have been accepted as first-line treatment in refractory heart failure, but a lack of response is a frequent event. A randomised single blind study was performed to evaluate the effects of the combination of high-dose furosemide and small-volume hypertonic saline solution (HSS) infusion in the treatment of refractory NYHA class IV congestive heart failure (CHF). Sixty patients (21 F/39 M) with refractory CHF (NYHA class IV) of different etiologies, unresponsive to high oral doses of furosemide, ACE-inhibitors, digitalis, and nitrates, aged 65-90 years, were enrolled. They had to have an ejection fraction (EF) <35%, serum creatinine <2 mg/dl, BUN </=60 mg/dl, a reduced urinary volume and a low natriuresis. The patients were randomised in two groups (single blind): group 1 (11 F/19 M) received an i.v. infusion of furosemide (500-1000 mg) plus HSS (150 ml of 1.4-4.6% NaCl) b.i.d. in 30 min. Group 2 (10 F/20 M) received an i.v. bolus of furosemide (500-1000 mg) b.i.d., without HSS, during a period lasting 6-12 days. Both groups received KCl (20-40 mEq.) i.v. to prevent hypokalemia. All patients underwent at entry a physical examination, measurement of body weight (BW), blood pressure (BP), heart rate (HR), evaluation of signs of CHF, and controls of serum Na, K, Cl, bicarbonate, albumin, uric acid, creatinine, urea and glycemia and daily during hospitalization, as well as the daily output of urine for, Na, K and Cl measurements. Chest X-ray, ECG and echocardiogram were obtained at entry during and at the discharge. During the treatment and after discharge the daily dietary Na intake was 120 mmol with a drink fluid intake of 1000 ml daily. An assessment of BW and 24-h urinary volume, serum and urinary laboratory parameters, until reaching a compensated state, were performed daily, when i.v. furosemide was replaced with oral administration (250-500 mg/day). After discharge, patients were followed as outpatients weekly for the first 3 months and subsequently once per month. The groups were similar for age, sex, EF, risk factors, treatment and etiology of CHF. All patients showed a clinical improvement. Six patients in both groups had hyponatremia (from 120 to 128 mEq./l) at entry. A significant increase in daily diuresis in both groups was observed (from 390+/-155 to 2100+/-626, and from 433+/-141 to 1650+/-537 ml/24 h, P<0.05). Natriuresis (from 49+/-15 to 198+/-28 mEq./24 h) was higher in group 1 vs. group 2 (from 53.83+/-12 to 129+/-39 mEq./24 h, P<0.05). Serum Na (from 135.9+/-6.8 to 142.2+/-3. 8 mEq./l, P<0.05) increased in the group 1 and decreased in the group 2 (from 134.7+/-7.9 to 130.1+/-4.3 mEq./l). Serum K was decreased (from 4.4+/-0.6 to 3.9+/-0.6, and 4.6+/-9 to 3.6+/-0.5 mEq. /l, P<0. 05) in both groups. BW was reduced (from 73.8+/-9.1 to 63. 8+/-8.8, and from 72.9+/-10.2 to 64.5+/-7.5 kg, P<0. 05) in both groups. Group 2 showed more patients in NYHA class III than group 1 (18 vs. 2 patients, P<0.05). Group 2 showed an increase of serum creatinine. Serum uric acid increased in both groups. BP values decreased, and HR was corrected to normal values in both groups. Group 2 showed a longer hospitalization time than group receiving HHS infusion (11.67+/-1.8 vs. 8.57+/-2.3 days, P<0.001). In the follow-up (6-12 months), none of the patients from group 1 were readmitted to the hospital and they maintained the NYHA class achieved at the discharge. Group 2 showed 12 patients readmitted to hospital and a higher class than at discharge. Our data suggest that the combination of furosemide with HSS is feasible and it appears that this combination produces an improvement of hemodynamic and clinical parameters, reduces the hospitalization time and maintains the obtained results over time in comparison with those receiving high-dose furosemide as bolus.

Evans formula

The Evans formula was the first burn resuscitation formula based on body surface area damage and body weight, described in 1952. It was the standard burn care formula for years. Formula Evans formula: normal saline at 1 ml/kg/% TBSA burn " colloid at 1 ml/kg/% TBSA burn. For second 24 hours, give half of the first 24-hour requirements " D5W (dextrose 5% in water) 2000 ml. References Emergency medical procedures

InternalMed_Harrison

from as little as 15 min after injection to 60 min after oral administration. When given in a dose that normalizes 24-h urinary osmolarity (400–800 mosmol/L) and volume (15–30 mL/kg body weight), DDAVP produces a slight (1–3%) increase in total body water and a decrease in plasma osmolarity/sodium that rapidly eliminates thirst and polydipsia (Fig. 404-5). Consequently, water balance is maintained within the normal range. Hyponatremia does not develop unless urine volume is reduced too far (to less than 10 mL/kg per day) or fluid intake is excessive due to an associated

Fluid Management -- Preparation

Another commonly used formula predicts fluid requirements over 24 hours. The following example shows an application of this formula: First 10 kg: 100 mL/kg/d Next 10 to 20 kg: Additional 50 mL/kg/d Any remaining weight more than 20 kg: Additional 20 mL/kg/d For example, the maintenance fluid requirements of an adult man whose body weight is 70 kg man are calculated as follows: First 10 kg: 100 mL/kg/d x 10 kg = 1000 mL/d Next 10 to 20 kg: 50 mL/kg/d x 10 kg = 500 mL/d Remaining 50 kg: 20 mL/kg/d x 50 kg = 1000 mL/d Total fluids per day: 1000 + 500 + 1000 = 2500 mL/d Hourly fluid rate: 2500/24 = 104 mL/h

[Hyponatremia and hypernatremia in the elderly].

The study aimed at evaluating an incidence of hypo- and hypernatremia in the elderly and the results of therapy. Hyponatremia. The studies involved 18 patients aged 69.8 +/- 5.9 years with hyponatremia of 126.8 +/- 2.7 mmol/L. The main causes of hyponatremia were: diuretics, diarrhoea, and vomiting. Sodium deficit was calculated prior to the treatment in all patients. An analysis of hyponatremia incidence indicates that hyponatremia was diagnosed in 1.39% of patients over 60 years, hospitalized within 1989-1990. Sodium deficit in this group was 495.5 +/- 167.7 mmol. Sodium chloride solution was given intravenously to 12 patients, according to the "free correction" principle (a mean increase in serum sodium level was 0.17 +/- 0.07 mmol/L per hour). Mortality in such treated patients was 33%. Sodium chloride was not given to 6 out of examined patients. In 12 patients (66.6%) hyponatremia developed prior to hospitalization, in 6 patients (33.3%) during hospitalization. Mortality rate was 16.6% and 50%, respectively. This confirms higher mortality rate of the rapidly developing hyponatremia in the hospitalized elderly patients. In some cases hyponatremia may constitute iatrogenic complication, especially in the elderly given diuretics in an uncontrollable way. Own experience suggests that elderly patients with a risk of hyponatremia require close monitoring and early compensation of the electrolyte disorders. Hypernatremia. The studies involved 20 patients aged 71.4 +/- 7.7 years with hypernatremia of 155.6 +/- 8.4 mmol/L. A total water deficit (DH20) was calculated in this group. An analysis of hypernatremia incidence showed that this state was diagnosed in 1.55% of patients treated at the Department of Arterial Blood Hypertension within 1989-1990. Total water deficit was 3.9 +/- 1.9 L. A 5% glucose was given intravenously to 15 patients whereas oral fluid therapy was carried out in 5 patients. A mean corrected DH2O in the first day was 46.0 +/- 21.0%. Mortality rate in this group was 65%. It is worth mentioning that 37% of patients with chronic hypernatremia which developed prior to hospitalization died while in case of the acute hypernatremia developed in the hospital mortality rate was 83%. A significant effect on the results of therapy plays an early correction of hypernatremia. Mortality rate in case of DH2o supplementation below 30% during the first 24 hours is about 66%., if DH2o supplementation is 31-60%, a mortality rate is 63%, and in DH2o supplementation over 60% mortality rate is 100%. The obtained results suggest that hypernatremia in the elderly is related to the high mortality rate (65%). An early decrease of water deficit increases mortality rate in patients with hypernatremia.

Syndrome of inappropriate antidiuretic hormone secretion

Treatment How to manage SIADH depends on whether symptoms are present, the severity of the hyponatremia, and the duration. Management of SIADH includes: Removing the underlying cause when possible. Mild and asymptomatic hyponatremia is treated with adequate solute intake (including salt and protein) and fluid restriction starting at 500 ml per day of water with adjustments based on serum sodium levels. Long-term fluid restriction of 1,200–1,800 mL/day may maintain the person in a symptom free state. Moderate and symptomatic hyponatremia is treated by raising the serum sodium level by 0.5 to 1 mmol per liter per hour for a total of 8 mmol per liter during the first day with the use of furosemide and replacing sodium and potassium losses with 0.9% saline. For people with severe symptoms (severe confusion, convulsions, or coma) hypertonic saline (3%) 1–2 ml/kg IV in 3–4 h should be given. Drugs

Effect of 50 milliliters of 50% dextrose in water administration on the blood sugar of euglycemic volunteers.

To evaluate the effect of administration of 1 ampule of 50% dextrose in water solution (D50W) on serum glucose levels in healthy adult volunteers, the authors set out to determine whether a pre-D50W serum glucose level can be predicted from the ED sample. This was a prospective, interventional study conducted from the ED of an urban, university-affiliated hospital. All subjects were healthy employee volunteers between 25 and 40 years of age. Baseline serum glucose levels were determined and all subjects were given an i.v. bolus of 25 grams of 50% dextrose solution. The main outcome measures were post-D50W serum glucose levels (observed) at 5 predetermined time intervals (5 min, 15 min, 30 min, 1 hr, and 2 hr). An expected change in serum glucose was calculated using the volume of distribution formula for glucose. Twenty-five volunteers (17 males and 8 females) participated in the study. The mean baseline serum glucose was 82.3 +/- 13.5 mg/dL. The mean post-infusion levels were: 244.4 +/- 44.6 mg/dL (5 min), 145.8 +/- 52.3 mg/dL (15 min), 88.1 +/- 28.8 mg/dL (30 min), 77.6 +/- 13.6 mg/dL (60 min), and 83.2 +/- 11.4 mg/dL (120 min). Using a mixed-effect regression model, statistically significant increases in serum glucose levels were found at 5 minutes (p < 0.001) and 15 minutes (p < 00001) following administration of D50W. There was a return to baseline serum glucose by 30 minutes. The expected change based on the volume of distribution formula (53.7 +/- 34.9) did not correlate with the observed changes at any measured time interval. Without pre-intervention blood drawing by emergency medical services, it is not possible to accurately predict pre-D50W serum glucose levels based on post-D50W glucose levels. The diagnosis of hypoglycemia as the etiology of altered mental status must therefore remain a diagnosis of exclusion. In addition, the return of serum glucose to baseline after 30 minutes suggests the duration of the effect of 1 ampule of D50W. Frequent re-evaluation of the serum glucose levels of suspected or proven hypoglycemic patients after administration of D50W should be considered.

Ranson criteria

Acute pancreatitis not secondary to gallstones At admission: Blood glucose > 11.11 mmol/L (> 200 mg/dL) Age > 55 years Serum LDH > 350 IU/L Serum AST > 250 IU/L WBC count > 16000 cells/mm3 Within 48 hours: Serum calcium < 2.0 mmol/L (< 8.0 mg/dL) Hematocrit decreased by > 10% Oxygen (hypoxemia with PaO2 < 60 mmHg) BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration Base deficit (negative base excess) > 4 mEq/L Sequestration of fluids > 6 L Acute pancreatitis secondary to gallstones At admission: Glucose > 220 mg/dl Age > 70 years LDH > 400 IU/L AST > 250 IU/ 100 ml WBC count > 18000 cells/mm3 Within 48 hours: Serum calcium < 8 mg/dL Hematocrit decreased by > 10% Base deficit > 4 mEq/L BUN increased by > 2 mg/dL Sequestered fluid > 6L

Hypernatremic diarrheal dehydration treated with oral glucose-electrolyte solution containing 90 or 75 mEq/L of sodium.

Of 33 infants with hypernatremic dehydration (serum Na+ of greater than or equal to 150 mEq/L) 7 were excluded, 6 because severe alteration of the level of consciousness or shock precluded oral rehydration and 1 because he was given glucose-electrolyte solution plus water. We studied the remaining 27 infants. Twenty (group A) were treated with the World Health Organization-recommended oral rehydration solution (90 mEq/L Na+) and seven (group B) were treated with Pedialyte-RS (Abbott Laboratories Ltd.; 75 mEq/L Na+). The rehydrating solutions were administered in a volume equivalent to twice the clinically estimated fluid deficit. Initial serum sodium was 156.7 +/- 0.9 mEq/L for group A and 155.8 +/- 1.8 mEq/L for group B (mean +/- SEM). The mean time to achieve rehydration was 14.3 and 16.6 h for groups A and B, respectively. Twenty-four hours after commencing oral rehydration, serum Na+ had decreased to 144.8 +/- 1.8 mEq/L for group A and 144.5 +/- 0.9 mEq/L for group B. In two patients in group A, the serum Na+, which, had not decreased to less than 150 mEq/L at 24 h, did so at 48 h. Only in one case (group A) did the serum Na+ increase. This patient had high stool output and failed to become rehydrated after 24 h of unsuccessful oral rehydration. None of the patients had seizures or persistent CNS dysfunction. We conclude that the slow administration of oral rehydration solutions containing either 90 or 75 mEq/L Na+ is a safe and effective treatment of hypernatremic dehydration.

Shock (circulatory)

Fluids Aggressive intravenous fluids are recommended in most types of shock (e.g. 1–2 liter normal saline bolus over 10 minutes or 20 ml/kg in a child) which is usually instituted as the person is being further evaluated. Colloids and crystalloids appear to be similar with respect to outcomes., Balanced crystalloids and normal saline also appear to be similar in critically ill patients. If the person remains in shock after initial resuscitation, packed red blood cells should be administered to keep the hemoglobin greater than 100 g/l. For those with hemorrhagic shock, the current evidence supports limiting the use of fluids for penetrating thorax and abdominal injuries allowing mild hypotension to persist (known as permissive hypotension). Targets include a mean arterial pressure of 60 mmHg, a systolic blood pressure of 70–90 mmHg, or until their adequate mentation and peripheral pulses. Hypertonic fluid may also be an option in this group. Medications

A double-blind clinical trial comparing World Health Organization oral rehydration solution with a reduced osmolarity solution containing equal amounts of sodium and glucose.

To compare the safety and efficacy of an oral rehydration solution (ORS) containing 75 mmol/L of sodium and glucose each with the standard World Health Organization (WHO) ORS among Egyptian children with acute diarrhea. One hundred ninety boys, aged 1 to 24 months, who were admitted to the hospital with acute diarrhea and signs of dehydration were randomly assigned to receive either standard ORS (311 mmol/L) or a reduced osmolarity ORS (245 mmol/L). Intake and output were measured every 3 hours. In the group treated with reduced osmolarity ORS, the mean stool output during the rehydration phase was 36% lower (95% confidence interval, 1%, 100%) than in those treated with WHO ORS. The relative risk of vomiting during the rehydration phase was significantly lower in children treated with reduced osmolarity ORS (relative risk, 2.4; 95% confidence interval, 1.2, 4.8). During the maintenance phase, stool output, mean intake of food and ORS, duration of diarrhea, and weight gain were similar in the treatment groups. The relative risk of treatment failure (need for unscheduled administration of intravenous fluids) was significantly increased in children receiving standard WHO ORS (relative risk, 7.9; 95% confidence interval, 1.1, 60.9). The mean serum sodium concentration at 24 hours was significantly lower in children receiving the reduced osmolarity ORS solution (134 +/- 6 mEq/L) than in children receiving the standard WHO ORS (138 +/- 7 mEq/L) (p < 0.001). The relative risk of the development or worsening of hyponatremia was not increased in children given the reduced osmolarity ORS, and urine output was similar in the treatment groups. The reduced osmolarity ORS has beneficial effects on the clinical course of acute diarrhea in children by reducing stool output, and the proportion of children with vomiting during the rehydration phase, and by reducing the need for supplemental intravenous therapy. These results provide support for the use of a reduced osmolarity ORS in children with acute noncholera diarrhea.

First_Aid_Step2

Assess volume status by conducting a clinical exam and measuring urine volume and osmolality. Hypertonic Na+ gain: Due to hypertonic saline/tube feeds or ↑aldosterone (suppresses ADH). Pure water loss: Due to central or nephrogenic diabetes insipidus; characterized by large volumes of dilute urine. Do not neglect dermal and respiratory insensible losses. Hypotonic f uid loss: Due to ↓ intake, diuretics, intrinsic renal disease, GI losses (diarrhea), burns, and osmotic diuresis (mannitol, glucose in DKA, urea with high protein feeds). A minimal volume (approximately 500 ml/day) of maximally concentrated urine (> 800 mOsm/kg) suggests adequate renal response without adequate free-water replacement. Treat the underlying causes and replace free-water deficit with hypotonic saline, D5W, or oral water, depending on volume status.

Normal Saline -- Administration

Remaining 30 kg weight = 750 mL (25 mL/kg x 30) Total = 2250 mL/day or 94 mL/hr First 10 kg weight = 4 mL/kg/hr x 10 = 40 mL/hr Second 10 kg weight = 2 mL/kg/hr x 10 = 20 mL/hr Remaining 30 kg weight = 1 mL/kg/hr x 30 = 30 mL/hr Total = 90 mL/hr

InternalMed_Harrison

The therapeutic goals in hypovolemia are to restore normovolemia and replace ongoing fluid losses. Mild hypovolemia can usually be treated with oral hydration and resumption of a normal maintenance diet. More severe hypovolemia requires intravenous hydration, tailoring the choice of solution to the underlying pathophysiology. Isotonic, “normal” saline (0.9% NaCl, 154 mM Na+) is the most appropriate resuscitation fluid for normonatremic or hyponatremic patients with severe hypovolemia; colloid solutions such as intravenous albumin are not demonstrably superior for this purpose. Hypernatremic patients should receive a hypotonic solution, 5% dextrose if there has only been water loss (as in diabetes insipidus), or hypotonic saline (1/2 or 1/4 normal saline) if there has been water and Na+-Cl– loss. Patients with bicarbonate loss and metabolic acidosis, as occur frequently in diarrhea, should receive intravenous bicar bonate, either an isotonic solution (150 meq of Na+-HCO3 in 5%


We believe that this question is open to challenge. Ibuprofen hepatitis is a rare adverse effect with a prevalence of about 3.7/100,000 users and 1.1/100,000 prescriptions. It appears that it may be related to dose and duration of treatment, but there is little evidence on this. Among the NSAIDs with the highest risk are diclofenac and sulindac. In terms of frequency, the prevalence of cholangiocarcinoma is 2/100,000 patients, a very comparable frequency. The absence of bile duct dilatation in cholangiocarcinomas can be seen in cases of intrahepatic cholangiocarcinomas or in those with mixed histology with hepatocarcinoma. It is true that the acute course and the absence of constitutional syndrome may make us think against this option and tip the balance towards ibuprofen hepatitis. Regarding the other options: acute cholangitis is characterized by the triad of jaundice, abdominal pain and fever; Gilbert's syndrome is an increase in bilirubin at the expense of indirectness.

We believe that this question is open to challenge. Ibuprofen hepatitis is a rare adverse effect with a prevalence of about 3.7/100,000 users and 1.1/100,000 prescriptions. It appears that it may be related to dose and duration of treatment, but there is little evidence on this. Among the NSAIDs with the highest risk are diclofenac and sulindac. In terms of frequency, the prevalence of cholangiocarcinoma is 2/100,000 patients, a very comparable frequency. The absence of bile duct dilatation in cholangiocarcinomas can be seen in cases of intrahepatic cholangiocarcinomas or in those with mixed histology with hepatocarcinoma. [HIDDEN] Regarding the other options: acute cholangitis is characterized by the triad of jaundice, abdominal pain and fever; Gilbert's syndrome is an increase in bilirubin at the expense of indirectness.

A 43-year-old male with no past history of interest consults for a ten-day history of jaundice of the skin and mucous membranes, choluria and acholia. He does not report abdominal pain, weight loss or other symptoms, except generalized pruritus. She denies alcohol consumption. She does not take any medication except occasional ibuprofen for muscle pain after sports activities. The CBC shows increased bilirubin at the expense of direct bilirubin. An urgent ultrasound shows a normal liver, vesicular cholesterosis and absence of bile duct dilatation, with no other alterations of interest. What is the most likely diagnosis?

Biliary Obstruction -- History and Physical -- History and Presentation

A careful history of symptom duration, if gradual or acute onset, accompanying symptoms like weight loss, loss of appetite, nausea/vomiting is important. Similarly, any right-sided abdominal pain, along with severity and radiation, is important to know. History of diarrhea, hematochezia, and upper GI bleeding symptoms is also relevant to diagnosing the underlying process. It is imperative to know any pertinent personal and family history like bile duct or pancreatic malignancy, inflammatory bowel disease, or primary liver disease. A careful review of social history related to current and former smoking, alcohol use, and drug abuse is important. Similarly, travel history to parasitic endemic regions is of value in determining the etiology of biliary obstruction. A careful review of medication history can sometimes be of great significance in determining intrahepatic cholestasis vs. extrahepatic biliary obstruction.

Hydralazine-induced cholestatic hepatitis.

Hydralazine has been widely used for treating hypertension, particularly in patients with renal failure. We report a case on a patient in whom we believe the drug was implicated in an otherwise unexplained disturbance of liver function. A 63-year-old African-American female with medical history of hypertension and end-stage renal disease (on hemodialysis) was admitted to the hospital with epigastric pain and jaundice. The symptoms started about 1 week ago. Initial laboratory tests showed abnormal liver enzymes with elevated conjugated bilirubin and alkaline phosphatase suggestive of cholestatic jaundice. Amylase and lipase were normal. Abdominal ultrasound showed normal caliber common bile duct without evidence of obstruction. Abdominal CT scan does not show any evidence of intra- or extrahepatic biliary ductal dilatation, and no mass lesions were seen in the pancreas. Further blood chemistry showed worsening of liver enzymes and increased bilirubin over the next 2-3 days. Magnetic resonance cholangiopancreatography failed to show any evidence of intra- or extrahepatic biliary ductal dilatation. No other laboratory evidence of cholestatic jaundice was found. Before proceeding for invasive diagnostic procedure, that is, endoscopic retrograde cholangiopancreatography, the patient's drug history was reviewed. She was on hydralazine 75 mg 3 times per day, started 5 months ago. At that time, her liver function tests were normal. As we could not find any other cause of cholestatic jaundice, we attributed this as a side effect of hydralazine. A trial was given by stopping the hydralazine. It was seen that there was significant improvement in the liver function enzymes over the next week. Complete clinical and biochemical recovery occurred over the next 4 weeks. Liver injury after long-term therapy with hydralazine and after short-term therapy with hydralazine (2-10 days) has been described. Hydralazine-induced hepatotoxicity may manifest as hypersensitivity-type injury, mixed hepatocellular injury, acute hepatitis, cholestatic jaundice, or centrilobular necrosis. The Hydralazine-induced cholestatic liver injury seems to be fully reversible. Complete clinical and biochemical recovery occurs after discontinuation of the drug. Also, the differential diagnosis of any patient with hepatocellular injury should include medications. This will prevent unnecessary diagnostic tests.

Diagnosing alcoholism.

Although the average physician can generally expect to see at least one alcoholic everyday, alcoholism is one of the most poorly diagnosed of the common illnesses. Alcoholism has supplanted syphilis as the great imitator of other diseases and produces measurable damage in every bodily system. The clues that the body presents, while not diagnostic in themselves, should alert physicians to the possibility of the alcoholism diagnosis. The author discusses some of the stereotypes and definitions that have added to the problem of reaching an alcoholism diagnosis, the importance of distinguishing between primary and secondary alcoholism, and the clues that may present both during a physician's history-taking session and in an examination. He concludes by discussing how to present the diagnosis to the patient.

Cholangiocarcinoma

Cholangiocarcinoma, also known as bile duct cancer, is a type of cancer that forms in the bile ducts. Symptoms of cholangiocarcinoma may include abdominal pain, yellowish skin, weight loss, generalized itching, and fever. Light colored stool or dark urine may also occur. Other biliary tract cancers include gallbladder cancer and cancer of the ampulla of Vater. Risk factors for cholangiocarcinoma include primary sclerosing cholangitis (an inflammatory disease of the bile ducts), ulcerative colitis, cirrhosis, hepatitis C, hepatitis B, infection with certain liver flukes, and some congenital liver malformations. However, most people have no identifiable risk factors. The diagnosis is suspected based on a combination of blood tests, medical imaging, endoscopy, and sometimes surgical exploration. The disease is confirmed by examination of cells from the tumor under a microscope. It is typically an adenocarcinoma (a cancer that forms glands or secretes mucin).

Alcoholic Liver Disease -- History and Physical -- Physical Examination

The clinical definition of alcoholic hepatitis is a syndrome of liver failure where jaundice is a characteristic feature; fever and tender hepatomegaly are often present. The typical presentation age is between 40 and 50 yrs, and it occurs in the setting of heavy alcohol use. Patients often report a history of intake of at least 30 to 50 g alcohol/day though over 100 g/day is common. Patients may be abstinent for weeks before admission. The cardinal sign is the rapid onset of jaundice. Other signs and symptoms include fever, ascites (SAAG greater than 1.1), and proximal muscle loss. Patients presenting with severe alcoholic hepatitis may have encephalopathy. Typically, the liver is enlarged and tender.

Clonorchis sinensis

Unusual cases of liver abscesses due to clonorchiasis have been reported. Liver abscesses may be seen even without dilatation of intrahepatic bile ducts. Symptoms While normally asymptomatic, most pathological manifestations result from inflammation and intermittent obstruction of the biliary ducts. The acute phase consists of abdominal pain with associated nausea and diarrhea. Long-standing infections consist of fatigue, abdominal discomfort, anorexia, weight loss, diarrhea, and jaundice. The pathology of long-standing infections consist of bile stasis, obstruction, bacterial infections, inflammation, periductal fibrosis, and hyperplasia. Development of cholangiocarcinoma is progressive.

Jaundice -- History and Physical -- History

Patients usually present with varying symptoms apart from yellowish discoloration of skin along with pruritus, thus providing clues to narrow down the etiology or can also be asymptomatic. A thorough questioning regarding the use of drugs, alcohol or other toxic substances, risk factors for hepatitis (travel, unsafe sexual practices), HIV status, personal or family history of any inherited disorders or hemolytic disorders is vital. Other important points include the duration of jaundice; and the presence of any coexisting signs and symptoms, like a joint ache, rash, myalgia, changes in urine and stool. [22] A history of arthralgias and myalgias before yellowing indicates hepatitis, either due to drugs or viral infections.

Secondary Sclerosing Cholangitis due to Gallbladder Adenocarcinoma.

Sclerosing cholangitis is a chronic cholestatic liver disease defined by both inflammatory and fibrotic changes of the biliary tract leading to diffuse stricture formation. This entity exists in both a primary and secondary form. Here we present a rare case of secondary sclerosing cholangitis due to direct metastasis from a gallbladder adenocarcinoma. A 55-year-old morbidly obese male presented electively with a 2-week history of low back pain and scleral icterus for 2 days. He also described severe epigastric pain that worsened postprandially and a 13 kg weight loss over the previous month. The patient denied any personal or familial history of malignancy or prior liver disease. Laboratory evaluation revealed mild elevation of transaminases with moderately elevated alkaline phosphatase and total bilirubin. Imaging included ultrasound and contrast-enhanced computed tomography of the abdomen and pelvis showing multiple large gallstones and a large tissue density mass within the fundus of the gallbladder. Subsequent endoscopic ultrasound was performed revealing celiac and portal lymphadenopathy with fine needle aspirations demonstrating adenocarcinoma. Over the next 15 days, bilirubin progressively increased. Magnetic resonance cholangiopancreatography was unremarkable. Liver biopsy, performed to exclude other etiologies of liver failure, demonstrated biliary cholestasis. Endoscopic retrograde cholangiopancreatography was then performed and an occlusion cholangiogram revealed diffuse multifocal stricturing of the intrahepatic bile ducts and moderate stenosis of the common bile duct without proximal ductal dilatation. Thus secondary sclerosing cholangitis due to gallbladder adenocarcinoma was diagnosed.

The Natural History of Alcoholism Revisited

Footnotes References

Epstein-Barr Virus Hepatitis Masquerading as Painless Jaundice.

Epstein-Barr virus (EBV) infection typically presents with pharyngeal symptoms and subclinical transaminitis. We present a case of a 27-year-old woman with no known past medical history who presented with painless jaundice and dark-colored urine for three days. Her review of systems was negative for fever, sore throat, nausea, vomiting, pruritus, or rash. Her last sexual contact was six months ago with a male partner, and she only drank alcohol socially. Family and surgical history were non-significant. Physical examination revealed 3+ bilateral conjunctival icterus without abdominal tenderness or organomegaly. She had elevated transaminases: alanine transaminase (ALT) of 1287U/L and aspartate aminotransferase of (AST) 1057U/L but her alkaline phosphatase (ALP) was only slightly above normal at 109U/L (normal range 35-104U/L), with a direct hyperbilirubinemia - total bilirubin 9.5mg/dl, direct bilirubin 6.8mg/dl; the abdominal ultrasound revealed non-dilated bile ducts. Hepatitis A, B, and C serology was negative, but her EBV serology showed an infection. She had incidental thalassemia minor without splenomegaly or asterixis. She was managed conservatively, and her liver enzymes trended down with supportive management. Although EBV is an uncommon cause of painless jaundice, this diagnosis should be considered, especially when other more common causes of jaundice have been ruled out. A high index of suspicion should be maintained to detect EBV hepatitis as it can easily be diagnosed through serological testing.

[How Johannes Brahms died].

In 1896, when he was 63 years old, Johannes Brahms, who had always been demonstrably in good health, developed an icterus of increasing intensity together with a considerable enlargement of the liver and loss of weight. Since infectious hepatitis could scarcely come into the question, from the medical point of view a neoplasm in the region of the liver as well as cirrhosis of the liver were considered. While hepatic carcinoma is a relatively rare disease in Europe even today and Brahms, on the other hand, had consumed copious quantities of concentrated alcoholic drinks during his lifetime, cirrhosis of the liver is the most probable diagnosis, especially as at the end hemorrhages from esophageal varices and the lower intestinal segments occurred.

Cases from the Osler Medical Service at Johns Hopkins University.

A 37-year-old woman presented with increasing abdominal pain and jaundice. Six weeks before admission, she developed persistent diarrhea and jaundice of the skin. She also bruised easily, and her gums bled. In the subsequent weeks, her appetite decreased, she was fatigued, and she had nausea, vomiting, and abdominal distension. She had a history of drinking 1 quart of vodka every day for 20 years, with brief periods of abstinence; she stopped consuming alcohol 11 days before admission because it no longer provided symptomatic relief. Her past medical history was also notable for depression, including a suicide attempt 4 years earlier. She did not smoke, use illicit drugs, or have unprotected sexual intercourse. She had received no blood transfusions and had not traveled recently. She took no medications, except for occasional ibuprofen. On physical examination, she was thin and deeply jaundiced, and she trembled and responded slowly to questions. She was afebrile but tachypneic, and she had orthostatic hypotension. Her HEENT examination was notable for scleral and sublingual icterus, as well as crusted blood on her gums and teeth. The jugular veins were flat. The cardiac examination revealed tachycardia (heart rate, 103 beats per minute) without murmurs, rubs, or gallops. The abdomen was nontender and protuberant, with hypoactive bowel sounds; the spleen was not palpable, and there was no fluid wave or caput medusae. The liver percussed to 18 cm, with a smooth edge extending 10 cm below the costal margin. She had cutaneous telangiectases on her chest and bilateral palmar erythema. There was no peripheral edema. The neurologic examination was notable for asterixis. Her stool was guaiac positive. Laboratory studies revealed the following values: hematocrit, 21.2%; white blood cells, 17,310/mm(3); ammonia, 42 micromol/L; serum creatinine, 3.9 mg/dL; serum urea nitrogen, 70 mg/dL; albumin, 2.1 g/dL; total bilirubin, 26.8 mg/dL; alanine aminotransferase, 14 U/L; aspartate aminotransferase, 77 U/L; alkaline phosphatase, 138 U/L; prothrombin time, 103 seconds (international normalized ratio, 10.6); and urinary sodium, <5 mg/dL. Urinalysis revealed an elevated specific gravity and numerous muddy granular casts. Hepatitis A, B, and C serologies were negative. On abdominal ultrasound examination, there was no ascites, and the liver was echogenic. The portal and hepatic veins were patent, and the hepatic arteries were normal. The spleen measured 14 cm. What is the diagnosis?

if the alcoholic's spouse ever complained of his drinking before they split. Interviews and questionnaires should always be backed up with interviews with the subject's family, with consultation of medical records, and with searches in public records for evidence of legal problems associated with drinking.

Diagnosis of ganglionar tuberculosis by endoscopic ultrasonography.

The endoscopic ultrasonography (EUS) is an endoscopic technique of proven clinical validity today, having a significant impact on the diagnosis and evaluation of several diseases with a low complication rate. The EUS-fine-needle aspiration (FNA) allows the evaluation of subepithelial lesions, extra-luminal lymph nodes or the gastrointestinal tract that are difficult to access by other methods with safe and high diagnostic accuracy. In the case reported, the EUS-FNA was useful for the differential diagnosis with residual biliary microlithiasis and the diagnosis of non-oncologic pathology. Male, white, 35-year-old, human immunodeficiency virus and tuberculosis treatment for about 5 months presented with jaundice. No fever, weight loss or abdominal pain. Choluria and hipocholia. History of cholecystectomy for about 1 year due to cholelithiasis. Laboratory tests showed cholestatic jaundice (direct hyperbilirrubinemia). Abdominal ultrasound showed liver without particularities, without biliary dilatation or filling defects. Initially suspected hepatitis due tuberculosis drugs so, the treatment was suspended. After a week with no drugs, no improvement in jaundice was observed. In contrast, a progressive increase indirect bilirubin. EUS performed with identification of mass along the distal common bile duct near the duodenal papilla. FNA performed with the presence of lymphocytes and tuberculosis bacile positive. After, endoscopic retrograde cholangiopancreatography was performed with sphincterotomy and placement of endoprosthesis for biliary drainage. The tuberculosis drugs were restarted with the plan to complete. The jaundice was resoluted. The patient completed 9 months of treatment and abdominal tomography has not identified a mass in that place. The EUS-FNA was proven to be a useful tool for diagnosis of non-oncologic pathologies like tuberculosis.

Eddi McKee

During her time in the show, it was hinted that Eddi liked to drink. Potts pointed out that drinking did appear to be the only way Eddi could deal with her many issues. Potts hoped the storyline would explored further, especially as Eddi's mother was an alcoholic. She also thought it would be fun to see Eddi lose her grip. Potts added that studies had shown people with alcoholics in their families became predisposed to it themselves.

Caroli Disease: A Presentation of Acute Pancreatitis and Cholangitis.

Caroli disease is a rare congenital disorder resulting from the dilation of large intrahepatic bile ducts. Patients affected with Caroli disease are at increased risk of complications resulting from bile stasis and stone formation. We report the case of a 37-year-old woman with a past surgical history of cholecystectomy who presented to the emergency room with a chief complaint of abdominal pain and nausea. The pain was characteristic of acute pancreatitis but she was hemodynamically stable. Total bilirubin was 4.1 mg/dL with a direct fraction of 3.1 mg/dL, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were 850 IU/L and 1025 IU/L, respectively. Serum amylase and lipase were elevated at 581 IU/L and 1328 IU/L, respectively. CT scan of abdomen/pelvis without contrast showed common bile duct (CBD) measuring 1.6 cm with intrahepatic biliary system dilation and mild peripancreatic fat stranding. She was diagnosed with acute pancreatitis. On the second day, she developed a temperature of 99.6°F. Hepatitis immunity panel was negative for acute hepatitis. The patient was started on antibiotics (IV ciprofloxacin and metronidazole) for suspicion of acute cholangitis. Endoscopic retrograde cholangiopancreatography (ERCP) was done which showed mild dilated intrahepatic ducts and CBD dilation of 1.6 cm, and a choledochal cyst at CBD. Sphincterotomy was done and good bile drainage was reported. She was later discharged in a stable condition. Caroli disease affects males and females equally and most are diagnosed before the age of 30 years correlated with the onset of symptoms. By far, the most commonly reported symptom is acute cholangitis but pancreatitis occurs rarely. Recurrent bouts of infection lead to portal hypertension, fibrosis of the liver and ultimately end up with an orthotopic liver transplant (OLT). Regular follow-ups are important for disease surveillance and monitoring.

Acute Pancreatitis -- History and Physical

The patient commonly describes moderate to severe abdominal pain in the epigastrium associated with nausea and anorexia. The nature of the pain can vary, depending on whether the etiology is a biliary obstruction or a metabolic/toxicologic cause. Biliary etiology is often described as a sharper pain that radiates to the back with a more acute onset. In contrast, metabolic and toxicologic causes like alcohol often have a more sluggish start with dull and generalized pain in the epigastrium. A detailed history regarding alcohol use and medications should be inquired about, keeping in mind that it takes over five years of heavy alcohol use to induce alcohol-related pancreatitis. Smoking history is also a significant risk factor for acute pancreatitis.

[Cancer of the middle third of the choledochus: an infrequent diagnosis].

We report the case of an 80-year-old woman with a previous history of HBP, hysterectomy due to cancer of the uterus and cholelithiasis, who was admitted in our hospital because of diffuse abdominal pain, marked jaundice, choluria and acholia during one week, together with anorexia and loss of weight. Blood chemistry results disclosed a total bilirubin of 11 mg/dl, a direct bilirubin of 8 mg/dl, GGTP 826 U/I, alkaline phosphatase 287 U/I, AST 285 U/I, ALT 837 U/I and LDH 242 U/I. The CA 19-9 marker was higher than 500 U/ml. The abdominal ultrasound examination did not show any space-occupying lesions; the extra and intrahepatic bile ducts were very dilated and the gall bladder showed multiple stones within its contents. The endoscopic retrograde cholangiopancreatography (ERCP) showed a homogeneous filiform defect at the middle third of the common bile duct of approximately 1 cm in length and with a marked dilatation of the bile ducts. A percutaneous drainage of the bile tree was performed, but the patient died.

[Medical aid in urgent alcohol-associated conditions].

The facts that the clinical manifestations of alcohol-associated urgent conditions are polymorphic, and that terms traditionally used by doctors to characterize these conditions are diverse, determine objective difficulties in rendering medical aid in such situations. However, the number of urgent alcohol-associated conditions grows every year. Analysis of diagnostic errors demonstrates that 30% of doctor's errors are subjective. Mistaken diagnosis is followed by casual treatment, independently on its cost and length. Treatment of alcohol-associated pathology is prerogative of general practitioners, which makes knowledge of clinical picture, terminology, legal aspects of rendering medical aid, expertise of the ability to work, and therapeutic tactics in urgent alcohol-associated conditions, important to doctors of all specialties.

Bilirubin

Very high levels of bilirubin may be caused by: Neonatal hyperbilirubinemia, where the newborn's liver is not able to properly process the bilirubin causing jaundice Unusually large bile duct obstruction, e.g. stone in common bile duct, tumour obstructing common bile duct etc. Severe liver failure with cirrhosis (e.g. primary biliary cirrhosis) Crigler–Najjar syndrome Dubin–Johnson syndrome Choledocholithiasis (chronic or acute). Cirrhosis may cause normal, moderately high or high levels of bilirubin, depending on exact features of the cirrhosis. To further elucidate the causes of jaundice or increased bilirubin, it is usually simpler to look at other liver function tests (especially the enzymes alanine transaminase, aspartate transaminase, gamma-glutamyl transpeptidase, alkaline phosphatase), blood film examination (hemolysis, etc.) or evidence of infective hepatitis (e.g., hepatitis A, B, C, delta, E, etc.). Jaundice

InternalMed_Harrison

Clinical Features The diagnosis of alcoholic liver disease requires an accurate history regarding both amount and duration of alcohol consumption. Patients with alcoholic liver disease can present with nonspecific symptoms such as vague right upper quadrant abdominal pain, fever, nausea and vomiting, diarrhea, anorexia, and malaise. Alternatively, they may present with more specific complications of chronic liver disease, including ascites, edema, or upper gastrointestinal (GI) hemorrhage. Many cases present incidentally at the time of autopsy or elective surgery. Other clinical manifestations include the development of jaundice or encephalopathy. The abrupt onset of any of these complications may be the first event prompting the patient to seek medical attention. Other patients may be identified in the course of an evaluation of routine laboratory studies that are found to be abnormal. On physical examination, the liver and spleen may be enlarged, with the liver edge being firm and

InternalMed_Harrison

agents can produce a picture of either acute hepatitis or cholestasis (Chap. 361). Equally important is a past history of unexplained “repeated episodes” of acute hepatitis. This history should alert the physician to the possibility that the underlying disorder is chronic hepatitis. Alcoholic hepatitis must also be considered, but usually the serum aminotransferase levels are not as markedly elevated, and other stigmata of alcoholism may be present. The finding on liver biopsy of fatty infiltration, a neutrophilic inflammatory reaction, and “alcoholic hyaline” would be consistent with alcohol-induced rather than viral liver injury. Because acute hepatitis may present with right upper quadrant abdominal pain, nausea and vomiting, fever, and icterus, it is often confused with acute cholecystitis, common duct stone, or ascending cholangitis. Patients with acute viral hepatitis may tolerate surgery poorly; therefore, it is important to exclude this diagnosis, and in confusing cases, a

Cholestatic jaundice due to ackee fruit poisoning.

A 27-yr-old Jamaican male presented with a 2-month history of jaundice, pruritus, intermittent diarrhea, and right upper quadrant abdominal pain. Over the next month, his abdominal pain and diarrhea improved, but his jaundice and pruritus worsened. He was afebrile and profoundly jaundice, with a benign abdominal examination. Medical workup included a normal abdominal ultrasound, iron studies, ceruloplasm, and serum electrophoresis. Negative viral (Epstein-Barr virus, cytomegalovirus, mononucleosis, hepatitis A, B, C) studies, ANA, AMA, ASMA, RPR were noted. He denied any alcohol, drug, or toxin exposure. Liver tests revealed total bilirubin of 25.6 mg/dl, direct bilirubin of 13.9 mg/dl, alkaline phosphatase 278 IU/L, AST 45 IU/L, and ALT 71 IU/L. Liver biopsy demonstrated centrilobular zonal necrosis and cholestasis most consistent with a toxic reaction. The patient was again interviewed regarding potential toxins, and he admitted to the ingestion of ackee fruit, a native Jamaican fruit that is illegal in the United States. Shortly after he had ceased intake of the fruit, his symptoms resolved and his liver function tests returned to normal. We present a case of chronic ackee fruit ingestion that led to cholestatic jaundice, vomiting, and abdominal pain.

Alcoholism

Historically the name "dipsomania" was coined by German physician C.W. Hufeland in 1819 before it was superseded by "alcoholism". That term now has a more specific meaning. The term "alcoholism" was first used in 1849 by the Swedish physician Magnus Huss to describe the systematic adverse effects of alcohol.

Choluria

Choluria is the presence of bile in urine. Choluria is a common symptom of liver diseases, such as hepatitis and cirrhosis. It can be described as dark or brown urine, often referred to as the color of Coca-Cola. Choluria is usually manifested when serum bilirubin is higher than 1.5 mg/dL. The presence of choluria is a useful symptom to distinguish if somebody presenting with jaundice has liver disease (direct hyperbilirubinemia) or hemolysis (indirect hyperbilirubinemia). In the first case, patients have choluria due to excess conjugated ("direct") bilirubin in blood, which is eliminated by kidneys. Hemolysis, on the contrary, is characterized by unconjugated ("indirect") bilirubin which is bound to albumin and thus not eliminated in urine. See too Acholia References External links Urinary bladder disorders

Pancreatitis -- History and Physical

In regards to medical history, healthcare providers should ask the patient specifically about the previous history of gallbladder disease, history of hyperlipidemia, and previous episodes of pancreatitis. A detailed social history should be obtained including a history of alcohol use. Clinicians should ask patients about recent procedures such as ERCP, and they should obtain a list of medications that the patient is currently taking. Patients should also be asked about a family history of pancreatic disorders.

Autoimmune hepatitis

Signs and symptoms Autoimmune hepatitis may present completely asymptomatic (12–35% of the cases), with signs of chronic liver disease, or acute or even fulminant hepatic failure. People usually present with one or more nonspecific, long-lasting symptoms such as fatigue, general ill health, lethargy, weight loss, mild right upper quadrant abdominal pain, malaise, anorexia, itching, nausea, jaundice or joint pain especially affecting the small joints. Rarely, rash or unexplained fever may appear. In women, the absence of menstruation (amenorrhoea) is a frequent feature. Physical examination may be normal, but it may also reveal signs and symptoms of chronic liver disease. Many people have only laboratory abnormalities as their initial presentation, as unexplained increase in transaminases and are diagnosed during an evaluation for other reasons. Others have already developed cirrhosis at diagnosis. Of note, alkaline phosphatase and bilirubin are usually normal.

Alcohol Use Disorder -- History and Physical

Patients may be asymptomatic or present with hypertension or insomnia in the early stages. In the later stages, as the condition progresses, patients may report additional symptoms such as nausea or vomiting, hematemesis, abdominal distension, epigastric pain, weight loss, jaundice, or other signs of liver dysfunction. To screen for AUDs, the US Preventive Services Task Force recommends the following tools: The 10-Question AUDIT (AUDs Identification Test) The 3-Question AUDIT (AUDIT-C) Single-Question Screening Test

Late cholestatic syndrome due to previous perforating trauma: Case report.

The presence of a foreign body obstructing the bile duct may appear through a typical picture of cholangitis, usually caused by the presence of gallstones. Male patient, 31 years old, involved an in accident with gunshot in 2006, injured in the abdominal region. Evolved to a picture of intense pain in the right hypochondrium, mainly after fat meals, without irradiation 12 years after being injured. Presented jaundice episode associated to fecal acholia, choluria, pruritus and sporadic fever. It was diagnosed cholangitis due to the foreign body like a bullet, located in the hepatic duct after tomography performed for investigation. The conduction of the case is described next. Cholestatic syndrome caused by gun bullet in a prior event to the symptoms is a rare event in the literature. Total, there are 8 case reports of bullets found in bile ducts with distinct evolution time among themselves. The first exam will not necessarily identify the bullet, but it simplifies the visualization of the bile ducts dilation, characterizing obstruction. The presence of a foreign body in the bile ducts is well reported in literature, and it is directly dependent on previous history. We should always avoid using cholangioresonance in dubious cases. To keep the ERCP as initial treatment is recommended due to the advances on the procedure quality, but in more severe cases or lack of resources, the surgical exploration is still indicated.

InternalMed_Harrison

The diagnosis of an alcohol use disorder ultimately rests on the documentation of a pattern of repeated difficulties associated with alcohol (Table 467-2). Thus, in screening, it is important to probe for marital or job problems, legal difficulties, histories of accidents, medical problems, evidence of tolerance, and so on, and then attempt to tie in use 5-Point Scale Item (Least to Most) 1. How often do you have a drink containing alcohol? 2. How many drinks containing alcohol do you have on a typical day? 3. How often do you have six or more drinks on one occasion? 4. How often during the last year have you found that you were not able to stop drinking once you had started? 5. How often during the last year have you failed to do what was normally expected from you because of drinking? 6. How often during the last year have you needed a first drink in the morning to get yourself going after a heavy drinking session? 7.

Cholangiocarcinoma

Signs and symptoms The most common physical indications of cholangiocarcinoma are abnormal liver function tests, jaundice (yellowing of the eyes and skin occurring when bile ducts are blocked by tumor), abdominal pain (30–50%), generalized itching (66%), weight loss (30–50%), fever (up to 20%), and changes in the color of stool or urine. To some extent, the symptoms depend upon the location of the tumor: people with cholangiocarcinoma in the extrahepatic bile ducts (outside the liver) are more likely to have jaundice, while those with tumors of the bile ducts within the liver more often have pain without jaundice.

Phillip Crosby

In his later years, Phillip's health was not good and he had problems with his back and knees following a motorcycle accident. In the 1980s, he was arrested several times for drunk driving and, despite 18 months of Alcoholics Anonymous, he told People, "I don't drink any more -- but I don't drink any less."