Critical Care BOOK Endocrine Disorders Chapters 44 & 56. SIADH, DI, & DK

Three major physiologic disturbances exist in DKA:

(1) hyperosmolality from hyperglycemia, (2) metabolic acidosis from accumulation of ketoacids, and (3) volume depletion from osmotic diuresis.

There are three goals in SIADH management:

(1) treating the underlying disease 2) alleviating excessive water retention (3) providing the comprehensive care needed when the patient has a depressed LOC.

hyperkalemia

- peaked T waves,

Hypokalemia

- ventricular ectopy, prolonged QT segments, depressed T waves

Initially, insulin administration involves giving an IV bolus of regular insulin at

0.15 units/kg body weight followed by a continuous infusion of regular insulin at a dose of 0.1 units/kg/hour (5 to 10 units/hour). This produces a steady decline in glucose concentrations at a rate of 65 to 125 mg/hour. An hourly insulin infusion of 0.14 units/kg/hour without initial bolus is sufficient to lower glucose and suppress hepatic ketone body production.

In DKA: Fluid replacement continues at roughly at _______/hr

1 L/hour until the heart rate, blood pressure, and urine flow indicate that hemodynamic stability is attained. Hypotonic solutions, such as 0.45% (half normal) saline solution, can be administered at a rate of 150 to 250 mL/hour after the intravascular volume has been restored, or if the serum sodium level is greater than 155 mg/dL.

Serum ADH

1-5 pg/mL

Labs DKA vs. HHS

1. The hyperglycemia in HHS is, by definition, a blood glucose level greater than 600 mg/dL; this is a significantly higher level than in DKA. Glucose can be in excess of 2,000 mg/dL. 2. Plasma osmolality is higher than in DKA and is reflective of more severe dehydration. In addition to extracellular sodium and water losses, a large additional "free water" deficit exists, probably because patients do not become thirsty, causing them to take in decreasing amounts of fluid. As a result, patients have very high serum levels of sodium and glucose. Serum osmolality is extremely high (greater than 310 to 320 mOsm/kg). 3. Patients may have some degree of ketosis as well but are usually nonketotic. In DKA, the degree of ketosis is much more severe. 4. In HHS, acidosis is not present or is very mild. In HHS, the anion gap attributable to ketoacids is usually less than 7 mEq/L. The patient may present with azotemia, hyperkalemia, and lactic acidosis.

Urine output and fluid intake

1.0-1.5 L/24 h

Urine specific gravity

1.005-1.030

With normal circulating blood volume and a normal glucose load, all this glucose is reabsorbed into the bloodstream. However, when the blood glucose level exceeds the normal threshold of about ______________________glucose begins to escape into the urine because the reabsorption capacity of the tubules is exceeded.

180 mg/dL,

When the plasma glucose reaches ____________________, it is necessary to decrease the insulin infusion to_____________________________

200 to 250 mg/dL, 0.5 units/kg/hour and add dextrose (5% or 10%) to the IV fluids. To prevent cerebral edema that may occur when the blood-brain barrier is affected by extreme fluid shifts, avoidance of hypoglycemia is warranted at this point. It is vital to start subcutaneous basal insulin 1 to 2 hours before IV insulin is stopped.

Serum osmolality

285-300 mOsm/kg

In severely symptomatic patients (SIADH) with acute hyponatremia, administration of

3% hypertonic saline solution and furosemide is used to correct hyponatremia in an emergency situation. Infusion of hypertonic saline solution at 0.1 mg/kg/minute prevents rapid volume overload and pulmonary edema. Usually, 300 to 500 mL given IV over 4 to 6 hours is appropriate.

Urine osmolality

300-1,400 mOsm/kg

Overall water loss in a 70 kg adult patient with DKA can be

5 to 8 L, or 15% of total-body water.

Ketoacids are excreted in the urine largely as sodium, potassium, and ammonium salts. This contributes to the third pathophysiologic problem of DKA: volume depletion and fluid and electrolyte loss as a result of osmotic diuresis. The fluid loss associated with DKA is approximately __________

6 L

The American Diabetes Association recommends bicarbonate replacement with severe acidosis as indicated by an arterial pH of

6.9 or less. It is also necessary to give bicarbonate when there is cardiac decompensation. The bicarbonate deficit can be calculated and replaced IV over several hours to raise the level at least to the 10 to 12 mEq/L range.

DI URINE

< 300mOsm/kg (URINE) Urine specific gravity is below 1.005

SIADH URINE

>300mOsm/kg (URINE!!!!!) Urine specific gravity is over 1.030

The syndrome of inappropriate antidiuretic hormone secretion (SIADH), is an excess of?

ADH

High serum osmolality=

Concentrated/ dehydrated!

Meds for SIADH

Conivaptan (Vaprisol) is an inhibitor of ADH that can be administered IV for hospitalized patients with euvolemic hyponatremia. It blocks vasopressin receptors in the renal collecting ducts to decrease water reabsorption. Demeclocycline, an antibiotic, has been effective because it interferes with the normal ADH effect in kidney tubules. Other medications that block the effects of ADH at the tubules include phenytoin (Dilantin), lithium, and fludrocortisone (Florinef).

HHS s/s

Dehydration; obtundation; hypothermia; toxic appearance; Kussmaul's respirations absent; nonketotic

DKA treatment protocol per class slides

Diagnosis: BS > 250, HCO3 < 15, venous pH < 7.3, + serum ketone level >1:4 Treatment: Fluids NS 500-1000 cc/hour x 2 hrs Then 0.45 NS at 250-500 cc/hr until BS < 250 When BS < 250, give D5/.45NS until DKA resolves Potassium Always get stat EKG in suspected DKA to r/o hyperkalemia If K > 5.5, treat K if symptoms of hyperkalemia, or if no symptoms check K q 2 hrs If K 4.0-5.5, give 20 meq K to each L of IV fluid If K 3-4, give 40 meq K to each L of IV fluid If K < 3, give PO K 10 meq PO q hr or 10 meq IV q hr, or as needed 20-40-10! Insulin IV regular insulin: 0.1 units/kg body weight bolus Then continuous insulin infusion at 0.1 units/kg/hr., accuchecks q 1 hr. When BS < 250 make sure you switch to D5/.45 NS Goal to reduce BG by 75-150 every hour

Rapid infusion of saline solution in DKA has possible complications. It can dilute plasma proteins and lower the osmotic pressure of the plasma. This allows?

Fluid to leak out of the vascular space through the capillary walls and contributes to the development of pulmonary edema or cerebral edema, particularly in children and older adults.

Sometimes a marked hyperglycemia and hyperosmolality without ketoacidosis develop in patients with diabetes; this is characteristic of________________.

HHS.

________________________which is gradual at first and then rapidly becomes more vigorous and more obvious as the arterial pH drops below 7.2, is a characteristic physical finding in DKA.

Hyperventilation/Kussmaul respirations.

Signs and Symptoms of Hypoglycemia

Hypothermia Tachypnea Tachycardia Dysrhythmias Hypertension Diaphoresis Tremulousness Hunger Nausea Belching Headache Personality changes Palpitations Blurred vision Combativeness, confusion, coma, convulsions

Tx for DI

Hypotonic IV solutions, such as 0.45% sodium chloride solution, are administered to match the urine output. A variety of replacement ADH (vasopressin) therapies are available. Desmopressin acetate is synthetic ADH that can be administered IV, orally, or as a nasal spray. Aqueous vasopressin (Pitressin) may be given as an IV bolus, continuous infusion, or subcutaneously

DI

Increased Serum Sodium, increased serum Osmolarity Dehydration Treatment ? Causes ?

HHS Tx

It is necessary to give low-dose insulin by continuous infusion (0.1 mg/kg/hour) because these patients are vulnerable to the sudden loss of circulating blood volume that occurs with higher doses of insulin and a rapid blood glucose reduction. As the glucose level returns close to normal (250 to 300 mg/dL), it is appropriate to stop the insulin infusion and add dextrose to the IV fluids to prevent a sudden drop in the blood glucose level. At this point, subcutaneous administration of insulin can proceed. Treatment of acute cerebral edema usually involves infusion of osmotic diuretic such as 20% mannitol.

Slide diagnosis for DKA

Ketonuria and glycosuria Hyperglycemia Metabolic acidosis Increased serum osmolality Elevated hematocrit levels High urine specific gravity Hyperkalemia or hypokalemia Hyponatremia or hypernatremia Increased anion gap

DKA Labs

Laboratory studies include blood glucose, chemistries, CBC with differential, osmolality, anion gap, pH, ABGs, urine acetone, and glucose. Possible findings include hyperosmolality, increased anion gap (greater than 7 mEq/L), decreased bicarbonate (less than 10 mEq/L), and decreased pH (less than 7.4). The serum glucose may range from 250 to 800 mg/dL or higher. Sodium, potassium, creatinine, and BUN levels are all ELEVATED. Magnesium and phosphate may also be high. Patients with DKA 881 often present with leukocytosis and the presence of greater than 10% neutrophil bands. The key diagnostic feature of DKA is the presence of serum ketones per the nitroprusside test or by direct measurement of β-hydroxybutyrate.8,15

Common Causes of Syndrome of Inappropriate Antidiuretic Hormone Secretion?

Malignancies • Bronchogenic carcinoma • Pancreatic adenocarcinoma • Prostate or thymus cancer • Leukemia CNS Causes • Head injury • Hemorrhage (subdural hematoma, subarachnoid hemorrhage) • Brain abscess • Infection, abscess, meningitis • Hydrocephalus Pulmonary Causes • Mechanical ventilation • Chronic obstructive pulmonary disease • Respiratory failure • Lung abscess, infection, pneumonia Medications • Nicotine • Opiates, morphine • Chlorpropamide, hypoglycemics, insulin • Antineoplastics • Tricyclic antidepressants, SSRIs • Anesthetics • Clofibrate • Diuretics Other Causes • Human immunodeficiency virus, AIDS • Senile atrophy • Pain • Fear • Myocardial infraction • Idiopathic

Serum Osmolality/ class slide

Normal level= 275-295mOsm/kg, Text has 285-300mOsm/kg (may use either range) Normal serum Na=133-145mEql/L Calculate serum osmolality= 2x Na level. *Example serum Na level of 120= Serum osmolality of 240 Low serum osmolality= fluid volume overloaded NOTICE THIS SAYS SERUM!!!! High serum osmolality= Concentrated/ dehydrated! Urine osmolality =300-1400mOsm/kg SNEAKING IN URINE OSM HERE! NOT SERUM!!!! SIADH >300mOsm/kg DI < 300mOsm/kg Urine Specific Gravity= Normal USG 1.005-1.030 In SIADH USG is high >1.030 DI < 1.005

Slide note DKA

Once treatment initiated, patient improvement is drastic Once blood glucose 200-259, then start D5W IV to replace stored glucose potassium only if becomes hypokalemic bicarb only in severe acidosis DKA Considered resolved when BG< 200 and pH < 7.3

Humulin REGULAR

Only form available for IV continuous infusion 0.5-1 2-3 5-8

risks for DKA Slide note

Risk: decrease in insulin intake, increase in dietary intake, decrease in routine exercies, growth spurts, surgery, infection, and trauma, emotional stress, insulin pump not working,

Dehydration (DI)

Vital signs are adversely affected, with severe tachycardia, hypotension, LOW CVP, and a possible rise in body temperature.

DKA

With insulin deficiency, the plasma glucose level rises. As illustrated in Figure 44-7, the concomitant effects of the counter-regulatory hormones, particularly cortisol and catecholamines, further aggravate hyperglycemia by enhancing gluconeogenesis, insulin resistance, and lipolysis. This leads to hepatic fatty acid oxidation to ketone bodies (β-hydroxybutyrate and acetoacetate), ketonemia, and metabolic acidosis.

The main laboratory abnormalities in SIADH are

a plasma hyponatremia and hypo-osmolality. The urine is simultaneously hyperosmolar, and there is a high excretion of urinary sodium. The urine specific gravity is high (concentrated), usually greater than 1.025, and the overall urinary output is lower (less than 30 mL/hour). Other laboratory findings include low BUN, creatinine, and uric acid levels; hypocalcemia and hypokalemia; and decreased hemoglobin and hematocrit values. The diagnosis can be confirmed by radioimmunoassay of plasma ADH, which is inappropriately elevated relative to plasma osmolality.

Diabetes insipidus can develop after

any event that causes edema or direct damage to the neurohypophysis. It can occur after head injuries, gunshot wounds, and lesions that disrupt blood supply to the area. Damage to the sphenoid bone, maxillofacial injuries, hypothalamic tumors, and nasopharyngeal tumors that invade the base of the skull may also lead to the development of diabetes insipidus. Direct trauma or ischemic events involving the hypothalamus, such as hemorrhage, infection, or neoplasm, may result in diabetes insipidus. Also, diseases or drugs that affect the renal collecting tubules may lead to diabetes insipidus. There is also a psychogenic polydipsia, in which excessive water is consumed, resulting in excess output.

The pathogenic processes associated with diabetes mellitus range from

autoimmune destruction of the islet beta cells of the pancreas (type 1 diabetes mellitus) to insulin resistance (type 2 diabetes mellitus).

DKA to Shock

blood is shunted away from many tissues, and the perfusion of nearly all tissues suffers. The resulting decrease in oxygen causes those tissues to shift to some degree of anaerobic glucose metabolism. This results in the increased production of lactic acid. The release of lactic acid into the circulation lowers the 880 bicarbonate further, aggravating the already existing metabolic acidosis.

Occasionally, the cause of SIADH is a pituitary tumor, but more commonly it occurs as the result of a?

bronchogenic (oat cell) or pancreatic carcinoma.

Major complications of diabetes insipidus are

cardiovascular collapse and tissue hypoxia. Seizures and encephalopathy can also result from fluid and electrolyte imbalance. Prognosis is excellent as long as the patient receives prompt and aggressive treatment.

One major complication (SIADH) to avoid is

central pontine myelinolysis. This may occur when correction of hyponatremia by hypertonic saline infusion is too rapid. Rapid correction of hyponatremia may lead to brain dehydration, cerebral bleeding, demyelination, neurologic injury, or death. Initial signs and symptoms include seizures, movement disorders, akinetic mutism, quadriparesis, and unresponsiveness. The best plan is to replace sodium at a rate NO FASTER than 1 to 2 mEq/L/hour to avoid the syndrome.

DKA is associated with less than 2% mortality rate overall, but it is a common cause of death due to

cerebral edema among children and adolescents with type 1 diabetes mellitus.13

When the serum sodium falls to less than 120 to 125 mEq/L, the more pronounced symptoms are?

cerebral edema, such as headache, nausea and vomiting, restlessness, muscular irritability, and seizures.

Drugs such as ________________ ________________ _____________&______________ (4) affect carbohydrate metabolism adversely and may lead to glucose impairment.

corticosteroids, thiazide diuretics, sedatives, and sympathomimetic

Diabetic ketoacidosis (DKA) is a

critical illness that manifests with severe hyperglycemia, metabolic acidosis, and fluid and electrolyte imbalances.

DI, involves a ?

deficiency of ADH

Medications administered for the treatment of diabetes insipidus include

desmopressin, aqueous pitressin, lysine vasopressin nasal spray, chlorpropamide (Diabinese), and clofibrate.

Polyuria, polydipsia, and dehydration are the hallmarks of

diabetes insipidus.

Diabetes insipidus is a

disease characterized by water imbalance resulting from inadequate ADH or resistance to ADH, leading to water diuresis and dehydration. Polyuria is the hallmark of the disorder: the kidneys can excrete great quantities of dilute urine, at times up to 20 L/d.

Physical evidence of hyponatremia includes?

dyspnea, jugular venous distention, restlessness, hypothermia, weight gain, mild to no edema, reduced and concentrated urine, anorexia, abdominal cramps, and disorientation.

Central diabetes insipidus is the more common condition that results in ADH deficiency; it responds favorably to

exogenous vasopressin administration.

Low serum osmolality=

fluid volume overloaded

As the vascular volume falls (DKA), glomerular filtration also falls. This decreasing renal function leads to increasing blood levels of

glucose, potassium, urea nitrogen, and creatinine. C PUG

SIADH is considered whenever the patient experiences?

hypotonic hyponatremia with elevated urine osmolality, the hallmark of the disorder.

The most common cause of DKA is:

infection, occurring in 30% to 50% of cases. Urinary tract infection (UTI) and pneumonia account for the majority of infections.8

In DKA , combined ___________________________&____________________________is a common finding.

lactic acidosis and ketoacidosis

anonin gap normal value?

less than 15 mEq/L.

A high anion gap means

metabolic acidosis

Usually, patients with HHS are

middle-aged or older (55 to 70 years), have undiagnosed type 2 diabetes, and are frequently residents of nursing homes.

hyperglycemia

polyuria, polydipsia, polyphagia, weight loss, and blurred vision.

The first step in managing SIADH is to

restrict fluid intake.

HHS criteria:

serum glucose greater than 600 mg/dL, arterial pH greater than 7.3, serum bicarbonate greater than 15 mEq/L, and minimal ketonuria and ketonemia.

DKA:As body phosphate stores are depleted, circulating plasma phosphate levels fall quite low, depriving the red blood cells of organic phosphate compounds. Under these circumstances, the red blood cells become depleted of certain key phosphate derivatives, increasing the?

tightness of oxygen binding to the hemoglobin in these cells. Therefore, less oxygen is given up, and tissue hypoxia worsens.

The classic example of the transient type of DI is illustrated by the patient undergoing a ____________________________for a hypophysectomy to remove a pituitary tumor.

transsphenoidal approach

A genetic predisposition for _________________________________ may exist: it appears that genetically predisposed patients contract the disorder after an environmental factor (viruses, congenital rubella, enteroviruses) triggers the autoimmune destruction of the islet cells,

type 1 diabetes

The immediate threat to life in a critically ill ketoacidotic patient is ?

volume depletion. After establishing an IV line, the nurse rapidly infuses 0.9% (normal) saline solution. The goal is to reverse the severity of the extracellular volume depletion and restore renal perfusion as soon as possible. **The first liter may be infused in 1 hour in patients with normal cardiac function; on average, the rate will be equal to 15 to 20 mL/kg body weight per hour.

Sudden and rapid lowering of the blood glucose with insulin allows

water to move very rapidly back into the cells and this can potentially lead to vascular collapse. Instead, early volume replacement should include sodium and water either before or along with insulin therapy.

Signs of Diabetic Ketoacidosis (DKA)

• Hyperventilation • Kussmaul's respirations and "fruity" breath • Lethargy, stupor, coma • Hyperglycemia • Glycosuria • Volume depletion • Hyperosmolality • Increased anion gap (>7 mEq/L)! • Decreased bicarbonate (<10 mEq/L)! • Decreased pH (<7.4)!

Treatment goals for the patient with DKA include the following:

• Improve circulatory volume and tissue perfusion • Correct electrolyte imbalances • Decrease serum glucose concentration • Correct ketoacidosis • Determine precipitating events.

Cardiac monitoring DKA

• Monitor vital signs hourly and PRN • Assess for dehydration/hypovolemia: tachycardia, decreased CVP and PAOP • Assess for hypervolemia: neck vein distention, pulmonary crackles and edema, increased CVP and PAOP • Administer vasopressor agents if hypotension is related to vasodilation Patient is free of dysrhythmias • Monitor ECG continuously • Evaluate and treat the cause of dysrhythmias (eg, acidosis, hypoxia, hypokalemia/hyperkalemia)