Metabolic Emergencies Diabetic Ketoacidosis Melanie S. Banaticla, RN,MAN Diabetic ketoacidosis (DKA) • DKA occurs predominantly in patients with Type 1 diabetes, but has been known to rarely occur in those with Type 2, typically in the presence of a coexisting acute illness Diabetic Ketoacidosis • Caused by an absence or markedly inadequate amount of insulin. • This results in disorders in the metabolism of carbohydrate, protein, & fat • Three main clinical features are: – Dehydration – Electrolyte loss – acidosis • It is an acute, life-threatening emergency associated with very high serum glucose levels and no insulin. • Due to the lack of insulin the body’s cells begin to starve, and after two or three days the body starts breaking down adipose tissue and proteins in an attempt to produce a usable energy source. This process is known as glyconeogenesis. The by-product of this process is an acid referred to as ketoacids. • The increase in circulating acids causes blood pH to fall leading to metabolic acidosis. When INSULIN is lacking… • The amount of glucose entering the cells is reduced. In addition, there is unrestrained production of glucose by the liver. • These lead to HYPERGLYCEMIA. • In an attempt to rid the body of excess glucose, the kidneys excrete the glucose along with water & electrolytes (Na & K). • This osmotic diuresis, characterized by polyuria leads to dehydration & marked electrolyte loss. • Patients with severe DKA may lose an average of 6.5 L of water & up to 400-500 mEq each of Na, K, & Chloride over 24 hour period. Another effect of INSULIN deficiency • Breakdown of fat (lipolysis) into free fatty acids & glycerol. • The free fatty acids are converted into ketones bodies by the liver. • In DKA there is an excess production of ketone bodies because of lack of insulin (that would normally prevent this from occuring). • KETONE BODIES are acids, & when they accumulate in the circulation they lead to METABOLIC ACIDOSIS. Signs & Symptoms • Hyperglycemia leads to polyuria & polydipsia (increased thirst) – Blurred vision, weakness, & headache – Orthostatic hypotension – Weak, rapid pulse Signs & Symptoms • The ketosis & acidosis characteristic of DKA lead to gastrointestinal symptoms such as: • Anorexia, n/v, & abdominal pain • Acetone breath (fruity odor) – occurs with elevated levels of ketone bodies. • Hyperventilation (kussmaul respiration) to decrease acidosis • Mental status may vary, may be alert, lethargic, or comatose Kussmaul Breathing • abnormally slow deep respiration characteristic of air hunger & occuring especially in acidotic states. Abnormal metabolism that causes s/sx of diabetic ketoacidosis Insulin lack ↑Breakdown of fat ↓Glucose utilization by the muscle, fat & liver ↑Fatty acids ↑Glucose production by liver Hyperglycemia Blurred vision Weakness headache polyuria Acetone breath Anorexia nausea n/v Abdominal pain ↑ketone bodies acidosis dehydration ↑respirations polydipsia Evidence of ketoacidosis • Low serum bicarbonate (0-15 mEq/L) • Low pH (6.8 to 7.3) • Low pCO2 (10-30 mm Hg) – reflects respiratory compensation (kussmaul respiration)for metabolic acidosis • Accumulation of ketone bodies is reflected in blood & urine ketone measurements. 3 main causes of DKA • 1. A decreased or missed dose of insulin • 2. An illness or infection – are associated with insulin resistance. • In response to physical & emotional stresses, there is an increase in the level of “stress” hormones – glucagon, epinephrine, norepinephrine, cortisol, & growth hormone. • These hormones promote GLUCOSE PRODUCTION by the liver & interfere with glucose utilization by muscle & fat tissue, counteracting the effect of insulin. • 3. The initial manifestation of undiagnosed & untreated diabetes Treatment • Aimed at correction of the three main problems: – Dehydration (rehydration) – Electrolyte loss (K infusion) – Acidosis ( insulin drip) For safe infusion of K, the nurse should check that: • There are no signs of hyperkalemia on the ECG (tall, peaked T waves) • The laboratory values of K are normal or low (N-4-4.5 mmol/L) • The patient is urinating (i.e, not experiencing renal shutdown) Prevention & Education “sick day rules” for managing DM when ill Guidelines to follow during periods of illness (“sick day rules”) • Take insulin or oral hypoglycemic agents as usual. • Test blood glucose and (for type 1 DM) test urine ketones every 3 to 4 hours. • Report elevated glucose levels (greater than 300 mg/dl) or urine ketones to the physician. • Insulin-requiring patients may need supplemental doses of regular every 3-4 hours. • If usual meal plan cannot be followed, substitute soft foods (e.g., 1/3 cup regular gelatin, 1 cup cream soup, ½ cup custard, 3 squares graham crackers) six to eight times per day. Guidelines to follow during periods of illness (“sick day rules”) • If vomiting, diarrhea, or fever persists, take liquids, (e,g., ½ cup regular cola or orange juice, ½ cup broth, 1 cup Gatorade) every ½ to 1 hour to prevent dehydration & to provide calories. • Report nausea, vomiting, & diarrhea to the physician because extreme fluid loss may be dangerous. • For patients with type 1 diabetes, inability to retain oral fluids may warrant hospitalization to avoid diabetic ketoacidosis & possibly coma. Hyperosmolar hyperglycemic nonketotic state (HHNK) Hyperosmolar hyperglycemic nonketotic state (HHNK) • HHNK is very similar to DKA in that it is a lifethreatening emergency caused by severe hyperglycemia. It is clinically different from DKA in that ketoacids are not formed and acidosis is usually minimal. • This is likely due to the patient producing enough insulin to adequately prevent glyconeogenesis • The typical HHNK patient is elderly with poorly controlled or undiagnosed Type 2 diabetes. • They often present with many symptoms which mimic those of DKA, including: • polydipsia, • polyuria, • weakness, • weight loss, • tachypnea (not Kussmaul respirations) and • tachycardia • Volume loss is significant in these patients due to increased urination and electrolyte imbalances, so look for signs of hypovolemia and dehydration including dry mucous membranes, orthostatic hypotension and sunken eyes • Volume loss is significant in these patients due to increased urination and electrolyte imbalances, so look for signs of hypovolemia and dehydration including dry mucous membranes, orthostatic hypotension and sunken eyes Hypoglycemia • Hypoglycemia is defined as a BGL of less than 80 mg/dl with symptoms consistent with a diagnosis of hypoglycemia which resolve after glucose administration. • However symptoms usually don’t appear until BGL are less than 60 mg/dl. Treatment • If the patient is alert and oriented enough to maintain their airway they can be given oral glucose 15g or an alternative such as a drink with sugar added. • If the patient is unable to obtain their own airway 1mg of glucagon can be given intramuscularly or subcutaneously, or establish an IV and administer 1g/ kg of a 50 percent dextrose in water solution (D50). • Due to the drug’s ability to cause thrombophlebitis, the dose for pediatric patients is 1cc/kg of a 25 percent solution, and a 10 percent solution is used in neonates. Of course, all doses are dependent on the paramedic’s local protocols. • When administering D50, the paramedic should consider administering thiamine as well, if it’s in their protocols. • Any patient with a history of alcohol intoxication or suspected malnourishment could be thiamine deficient. • Many patients treated for hypoglycemia are well aware of their condition and will refuse transport, and others will want to go for physician evaluation. • The paramedic should follow local protocol on patient refusals. If no transport is required, it is important that the patient eats a meal containing complex carbohydrates, as glucose is a simple sugar which is utilized quickly. Hyponatremia • Hyponatremia can be caused by salt-losing states, such as – vomiting or diarrhea, – diuretic excess, – adrenal insufficiency, or by excess total body water states such as: • the infection-induced syndrome of inappropriate secretion of antidiuretic hormone (SIADH), • nephrotic syndrome, and • cirrhosis. Factitious, or pseudohyponatremia, can occur with hyperglycemia, hyperlipidemia, or hyperproteinemia In infants, hyponatremia is commonly due to excess gastrointestinal loss from prolonged vomiting or diarrhea, or from inappropriately diluted formulas. Pyridoxine-dependent seizures are a rare cause of intractable seizures in neonates. Hyponatremia is typically defined as a serum sodium level less than 125 to130 mEq/L, although clinical symptoms are not usually seen until serum sodium falls below 120 mEq/L. Manifestations include: altered mental status, lethargy, vomiting, diarrhea, seizures, and circulatory collapse. Treatment • Treatment should be geared toward the underlying cause. Aggressive treatment with 3% hypertonic saline (514 mL/kg) should only be initiated if significant symptoms are present, such as seizures or coma. • A dose of 1048 KWON & TSAI5 mL/kg over 10 to 15 minutes should raise the sodium level by approximately 5 mEq/L; smaller additional doses of 2 to 3 mL/kg can be considered if there is no clinical improvement. Hepatic Encephalopathy Liver-largest internal organ in humans. Portal Veins • Vein that carries blood from the digestive organs, gall bladder, & spleen, especially the vein from the intestine carrying nutrient-rich food. Functions synthesis of proteins, immune and clotting factors, and oxygen and fat-carrying substances. Its chief digestive function is the secretion of bile, a solution critical to fat emulsion and absorption. The liver also removes excess glucose from circulation and stores it until it is needed. It converts excess amino acids into useful forms and filters drugs and poisons from the bloodstream, neutralizing them and excreting them in bile. The liver has two main lobes, located just under the diaphragm on the right side of the body. It can lose 75 percent of its tissue (to disease or surgery) without ceasing to function. terminologies • • • • • Hepatocyte – liver cells Sinusoid – small vessel in organ tissue Shunt – divert channel Varix or varices – swollen or knotted vein Collateral – additional Hepatic Encephalopathy • Definition: Cerebral dysfunction associated with severe liver disease. • Pathophysiology: – Inability of the liver to metabolize substances that can be toxic to the brain such as ammonia, which is produced by the breakdown of protein in the intestinal tract. Pathophysiology Etiology: Alcohol Abuse Malnutrition Infection Drugs Billiary Obstruction Destruction of HEPATOCYTES FIBROSIS/SCARRING Edema/ Ascites PORTAL HYPERTENSION Splenomegaly Anemia Development of collateral channels Caput medusae Obstruction of blood flow ↑pressure in the venous and sinusoidal channels Fatty infiltration FIBROSIS/SCARRING Portosystemic shunting of blood Increased pressure in capillaries arteries Esophageal varices Shunting of ammonia & toxins from intestine into the general circulation Hepatic Encephalopathy Sign and Symptoms: Lack of mental alertness to confusion Convulsion Asterexis Personality changes Decerebrate rigidity Coma Leukopenia CAPUT MEDUSAE Liver cirrhosis Medical Treatment • Restriction or elimination of dietary protein • Lactulose or neomycin to inhibit protein breakdown, decrease bacterial ammonia production, cleanse bowel of bacteria and protein. Nursing process Assessment • 1. mental status, LOC: lethargy progressing to coma. – Dullness, slurred speech – Behavioral changes, lack of interest in grooming or appearance • 2. Neurological exam: twitching, muscular incoordination, asterixis (a flapping tremmor) – arm-flapping caused by liver failure: • a recurrent flapping tremor of the arms, like the action of a bird's wings, that occurs as a result of a brain condition associated with liver failure. • 3. elevated serum ammonia level Early signs of encephalopathy • Restlessness • Slurred speech • Decreased attention span To decrease ammonia production • Reduce dietary protein to 20-40 g/day, maintain adequate calories. • Decrease ammonia formation in the intestine – Give laxatives, enemas as ordered – Administer lactulose (Cephulac) & neomycin (oral or rectal) as ordered. uremia Uremia • presence in the bloodstream of too many chemical wastes such as urea, a nitrogen-rich waste product attributable to extra protein in the diet. – As chemical wastes build up in the body they produce a toxic effect, possibly resulting in drowsiness, irritability, nausea, vomiting, breathlessness, headaches, and muscle cramps. • In extreme cases, uremia may cause convulsions, coma, or death. Uremia most commonly develops • when the kidneys fail to function properly. • when blood flow to the kidneys is reduced due to severe bleeding, serious burns, or heart attack. • when more wastes are formed in the bloodstream as a result of traumatic injuries or large surgical incisions. • kidney stone, a tumor in the urinary tract, or a severely enlarged prostate in males • Victims of uremia due to kidney failure undergo kidney dialysis, a medical procedure that removes wastes from the blood. • Transplantation of kidneys from healthy donors to uremic patients has also proven effective in some cases. Thanks…..
