Medical Emergencies Flashcards
What are some hematologic emergencies?
Sickle Cell Anemia
Hemophilia
Disseminated Intravascular Coagulation
Describe sickle cell anemia
Sickle cell anemia is a genetic disease that affects one in 500 African-Americans. It is also found in those of Mediterranean, East Indian, and Middle Eastern dissent.
2 genes are necessary for the disease to be present. If the individual has one gene, they have sickle cell trait.
Pathophysiology = development of HbS instead of HbA which creates red blood cells that are incapable of transversing the microcirculation.
What are some complications of sickle cell anemia?
Hepatomegaly Hepatic infarctions Jaundice Pulmonary emboli Core pulmonale Chronic skin ulcers Hemolytic anemia Cholelithiasis Cholecystitis Aseptic necrosis of bones Osteoporosis Priapism Cardiomegaly CHF Tachycardia Mesenteric infarcts Abdominal vessel infarcts CVAs
Where do the main types of sickle cell crisis occur?
Bone
Chest
Abdominal
Joints
What is acute chest syndrome?
Pulmonary micro-infarctions which can be complicated by infection.
Leading cause of mortality/morbidity in sickle cell patients.
What is the treatment for sickle cell crisis?
Hydration – normal saline (Be sure to watch for overload)
Analgesia (Do not use Demerol can be neurotoxic)
Oxygen
Partial exchange transfusion if PO2 < 60 mm Hg
Anti-emetics
Blood transfusions
Antibiotics
Folic acid supplements for aplastic crisis
Anti-inflammatories
Hydroxyurea - creates fetal hemoglobin
What are precipitating events that cause sickle cell crisis?
Infections Dehydration Hypoxemia Depression Fever Acidosis Anxiety Exposure to cold Travel in nonpressurized aircraft Sudden change in altitude
What chromosome carries the gene for Hemophilia?
X-recessive gene
Describe hemophilia A:
Lack of Factor VIII Occurs in males Minor bleeding episodes can lead to major sequelae. Arthritis. Treatment: FFP Cryoprecipitate Factor VIII DDAVP (D-Desaminoarginine) - stimulates the release of Factor VIII
Describe Hemophilia B:
Lack of Factor IX. Occurs in Males. Minor bleeding episodes can lead to major sequelae. Arthritis. Treatment: Antibody purified Factor IX FFP
Describe Von Willebrand’s Disease:
Occurs in women. Lack of Factor VIII Defective platelet adherence. Muco-cutaneous bleeding and heavy menstrual flow can be bad. Treatment: FFP Cryoprecipitate Factor VIII DDAVP Factor complex
Describe the pathophysiology of Disseminated Intravascular Coagulation:
Accelerated clotting triggers thrombosis which accelerates fibrinolysis causing platelets, fibrinogen, and clotting factors to be consumed faster than they can be replaced. The end result is simultaneous clotting and bleeding.
What are the manifestations of the thrombosis part of Disseminated Intravascular Coagulation?
Dysrhythmias Acrocyanosis Absent/unequal pulses Hypoxia Respiratory Distress Decreased Breath sounds Aphasia Unequal pupils Decreased Urine output Decreased bowel sounds Necrosis of extremities
What are the manifestations of the bleeding part of Disseminated Intravascular Coagulation:
Tachycardia Hypotension Bloody sputum Decreased breath sounds Decreased LOC Convulsions Dilated pupils Hematuria Enlarged kidneys Guaiac positive stools/emesis Abdominal hemorrhage Oozing from sites Ecchymosis
What are the lab values for disseminated intravascular coagulation?
PT/PTT - normal or decreased
Fibrinogen levels - decreased
Platelet levels - decreased
Fibrin Split products - increased
What is the treatment for Disseminated Intravascular Coagulation?
Heparin
Used when there is evidence of organ damage or loss of life/limb is imminent.
Blocks microthrombi formation.
Not recommended for CNS injury, Liver failure, Obstetrical events.
Antidote is Protamine Sulfate (can not give if have a fish allergy).
Treat underlying cause.
FFP - replace clotting factors.
Platelets
PRBC
Factor VIII
Cryoprecipitate
Relative vs. Absolute depletion of available insulin:
Relative: infection illness pregnancy stressors Absolute: non-compliant patient illness - fails to take insulin
Hyperglycemia causes both _____ and _____ _____ by osmosis. _______ are created from the use of fats and muscle proteins as a means to produce energy.
1) intracellular
2) extra cellular dehydration
3) Ketones
4 major problems with Diabetic ketoacidosis:
1) hyperglycemia
2) dehydration
3) Electrolyte Disturbances
4) Metabolic Acidosis
Lab Values for Diabetic Ketoacidosis:
Glucose - >300mg/dL UA - + glucose and Ketones pH - Acidotic Bicarbonate - decreased (<22) Acetone - Increased NaCl - decreased K - normal or elevated PCO2 - decreased BUN - Increased Creatinine - Increased Hgb - increased Hct - increased WBC - increased if infection present
Manifestations of Diabetic Ketoacidosis:
Lethargy Flushed skin Thirst Abdominal pain Hyporeflexia Anorexia Acetone breath Vomiting Blurred vision Orthostatic Hypotension Kussmaul respirations Fever Hypotension Tachycardia Poor skin turgor Weakness Dysrhythmias Polyuria History infection/illness Dry mucus membranes Mental status changes
Treatment of Diabetic Ketoacidosis:
Dehydration - fluid replacement When glucose is 250 switch to D5NS. Hyperglycemia - regular insulin Correct gradually Reduce glucose 75-100 per hour or can develop headache and cerebral edema. Electrolyte replacement: Hypokalemia can develop rapidly with treatment. Fluid replacement also depletes. Potassium replacements Acidosis: Bicarbonate if pH <7.0 - 7.1 Can cause rebound alkalosis can add to IV fluids
What is Hypersmolar Hyperglycemic Syndrome?
Hyperglycemic reaction in a non-insulin dependent diabetic.
What are some precipitating events for the development of hypersmolar hyperglycemic syndrome?
Pneumonia, G.I. bleed, MI, acute viral illness, subdural hematoma, pancreatitis, heat stroke, tube feedings without enough water, recent cardiac surgery, severe diarrhea/vomiting, UTI, sepsis, uremia, pulmonary embolism, CVA, burns, hyper alimentation, dialysis,
Medications: Thiazide diuretics, steroids, phenytoin, propanolol, Cimetidine, immunosuppressives.
What are the three major problems with hyperosmolar hyperglycemic syndrome?
Hyperglycemia
Dehydration
Hyperosmolality
Why are the presence of Ketones not noted with hyperosmolar hyperglycemic syndrome?
There is enough circulating insulin in order to avoid ketones.
What lab values are associated with hyperosmolar hyperglycemic syndrome?
Glucose – usually > 600, often > 1000
UA – Positive for glucose; negative for ketones
pH - normal (may be slightly acidotic)
PO2 - normal unless underlying respiratory problem.
WBC - increased if underlying problem infection.
Na - Normal or increased depending on dehydration.
K - normal or increased depending on dehydration.
Osmolality - increased.
Manifestations of hyperosmolar hyperglycemic syndrome:
Vague abdominal pain Polyuria Headache Seizures Shallow respirations Elevated T waves Anorexia Polydipsia Blurred vision Coma Tachycardia Dysrhythmias Confusion Nausea/vomiting
What is the treatment for hyperosmolar hyperglycemic syndrome?
Rehydrate
Oxygen
Foley
Potassium supplements to prevent hypokalemia from hemodilution and insulin therapy.
Cardiac monitor
Insulin drip not as important but is often used.
Heparin or Lovenox for blood viscosity.
What are some contributing factors to hypoglycemia?
Lack of intake. Increased physical stress. Liver disease Changes in medication. Pregnancy Alcohol ingestion Drugs - NSAIDs, phenytoin, thyroid, propanolol. Increased insulin intake Certain drugs – Salicylates / sulfonamides influence the metabolism of oral hypoglycemics
What is the pathophysiology of hypoglycemia?
When a decrease in glucose is sensed, the body releases glucagon and epinephrine. The glucagon releases stored glucose, but it cannot be utilized fast enough. The epinephrine decreases the utilization of existing glucose and may be the cause of the symptomatology that occurs.
Manifestations of hypoglycemia:
Confusion Seizures Slurred speech Cool & clammy Palpitations Shakiness Hunger Pale Competitiveness Coma Staggering gate Tachycardia Diaphoresis Dilated pupils Death
Treatment for hypoglycemia:
Glucose Oral - 10 to 15 g of carbohydrate followed by a meal. 4 to 6 ounces of orange juice 5 to 6 Lifesavers 1/2 to 3/4 cup of nondiet soda 6 ounces of milk 2 to 3 glucose tablets D50 Glucagon - IM (this will not work for a cirrhosis patient) Insulin Pump — turn off
What are the time frames for standard insulin peaks?
NovoLog, Apidra, Numalog = 30 to 90 minutes.
Humulin R, Novolin R = 2 to 4 hours.
Humulin N, Novolin N = eight hours.
Levimir, Lantus = no peak.
What is thyroid storm and what is the mortality rate?
Thyroid storm occurs in hyper thyroid patients who may either be undiagnosed or stop taking their medication. Mortality rate is 20 to 60%
What are some causes of hyper thyroidism?
Overactive thyroid – Grave’s disease.
Thyrotoxicosis - increased hormone release.
Drug induced - Iodine containing agents (amiodarone/lithium).
What are some manifestations of a thyroid storm?
Hyperthermia Tachycardia Tremors Exophthalmus Cardiac failure Hyperglycemia Hypertension Agitation Diaphoresis Mental status changes Pulmonary edema Hypercalcemia Metabolic acidosis Flushed skin
What is the treatment for thyroid storm?
General treatment:
Treat fever - no salicylates (causes more thyroid hormone to be released from binding sites).
Fluid replacement (hyperthermia/vomiting/diarrhea).
Anti-emetics
Antidiarrheals
Oxygen
Monitor/treat dysrhythmias
Do not allow shivering.
Treatment to slow release of hormone:
 Propanolol (large doses needed for tachycardia. Blocks conversion of T4 to T3).
Guanethidine/ Reserpine - depletes stores/blocks release.
Iodine (Give one hour after use of meds to block synthesis.)
Treatment to Block Synthesis of Hormone:
Propylthiouracil
Methimazole
Glucocorticosteroids/Diuretics
What is a myxedema coma?
Myxedema coma is a complication of hypothyroidism with a mortality rate of 50% (stated to be as high as 80%). It is a progressive disease process with respiratory failure as the usual cause of death.
What are the Etiologies of myxedema coma?
Autoimmune thyroiditis
Ablation therapy
Iodine deficiency
Tumor
Drugs (lithium, amiodarone, anticonvulsants)
Secondary hypothyroidism - pituitary dysfunction.
Tertiary hypothyroidism - hypothalamic dysfunction.
What are some precipitating factors of myxedema coma?
Infections General anesthesia Sedatives Antidepressants Trauma CHF Surgery Narcotics Cold temperatures Stress
How to tell the difference between hyperthyroid and hypothyroid:
Hyperthyroid = low TSH Hypothyroid = increased TSH
What are some manifestations of myxedema coma?
Hypothermia Decreased activity tolerance Weight gain Confusion Altered mental status Hypo ventilation Hyponatremia Decreased cardiac output Depressed T waves Myxedema madness Pronounced fatigue Dyspnea Tongue swelling Slow answers Coma Hypercarbia Decreased renal blood flow Peripheral vasoconstriction prolonged QT interval Dry, pale, cold skin
What is the treatment for myxedema coma?
ABC’s
Hormone replacement – T4 or T3
Glucocorticoids to prevent adrenal crisis in patients with compromised adrenal systems.
Passive warming.
What are the Etiologies for Addisonian Crisis (adrenal crisis)?
Disease state
Discontinuation of steroids
What are the Hallmark findings of Addisonian Crisis?
Hyponatremia
Hypoglycemia
Hyperkalemia
What are the manifestations of Addisonian Crisis?
N/P Amenorrhea Fever Irritability Abdominal cramps Hypovolemic shock Weakness Fatigue headache Tachycardia
What are some clues to a diagnosis of Addison’s disease?
Hyper pigmentation
Moon face
Truncal obesity
What is the treatment for Addisonian Crisis?
Fluids – used D5NS (Patient is hyponatremic and hypoglycemic).
Hydrocortisone
Mineralocorticoids (dexamethasone)
Treat for hyperkalemia - D50 and insulin but may resolve with fluids and glucocorticoids.
Cardiac monitoring
What are the five types of hepatitis?
Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E
What is the route for infection of hepatitis A?
Fecal – oral
What are the routes of infection for hepatitis B?
Percutaneous, sexual, Bile, perinatal
What are the routes of infection for hepatitis C?
Percutaneous, sexual, perinatal
What are the routes for hepatitis D?
*Occurs in combination with hep-B
Percutaneous, sexual, bile, perinatal
What is the route of infection for hepatitis E?
Fecal - oral.
*occurs in Underdeveloped countries
What are some manifestations of hepatitis?
Fever Anorexia Dark urine Jaundice Malaise N/V Abdominal pain Rash occurs with type B
What can chronic hepatitis C progress to?
Cirrhosis or carcinoma
