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.