A CASE PRESENTATION OF A PATIENT WITH DIABETIC KETOACIDOCIS (DKA) Prepared by: Tristan Villanueva Arcibal BSN-RN Presented on: July 16, 2013
DEMOGRAPHIC DATA • Name: Mr. X • Case no. :201--- • Age: 28 y/o • Gender: Male • Nationality: Saudi • Admission date: 11-4-2013 • Time of arrival: 0840H • Chief complaints: Persistent vomiting,Low blood pressure, High blood glucose, Altered mental status • Diagnosis: DKA
PHYSICAL ASSESSMENT • HEAD • Altered mental status ( restless and agitation) • GCS 12/15 • Eye response (3) : Responds to verbal command • Verbal response (4) : Confused • Motor response (5): Localizes pain • EYES • Pupils • Reactive to light • Round and equal in size
ENT • Dry oral mucosa • (+) Ketotic/ acetone breath • CHEST • Rapid breathing (30 cycles per minute) • Equal breath sounds • Symmetrical chest rise • No adventitious sounds (ex: wheezing, crackles) • HEART • Regular but rapid HR: 110 BPM • BP: 90/60 mmhg • S2> S1
ABDOMEN • (+) nausea and vomiting • Soft and non tender abdomen • Bowel sounds (+) • No signs of rebound tenderness, trauma & abdominal distention • GUT • Excessive urination • SKIN • Poor skin turgor
EXTREMITIES • Limbs are normal • (-) weakness, contractures, joint swelling/ paralysis
PAST MEDICAL HISTORY • Patient has Type 1 Diabetes Mellitus/ IDDM since 15 years with maintenance medication of Regular Insulin twice daily via subcutaneous route before meals.
PRESENT MEDICAL HISTORY • Patient was conveyed by Red Crescent Authority and was allegedly found unconscious inside his car. • Upon arrival to ER, patient was persistently vomiting, restless and disoriented . • Vital signs: BP 90/60 mmHG, PR 110 BPM, RR 30, Temp. 36.8 ,SPO2 98%, Blood Glucose 450 mg/dl. • Prior to confinement patient consumed large amount of alcohol and had failed to comply with his medication regimen.
Laboratory tests: • Glucose (random): 23.4 mmo/L (3.9-7.8 mmo/L) • Urinalysis : ++ketones • CBC • WBC: 9.04 (4.23-9.07) • HGB: 14.3 (13.7-17.5) • HCT: 39.6 (40.1-51.0) • PLT: 350 (163-337) • Electrolytes: • NA+: 141 mmO/L (135-150 mmO/L) • K+:4.3 mmO/L ( 3.5- 5.0 mmO/L) • Cl+ :98 mmO/L (98-111 mmO/L) • BUN: 4.42 mmO/L (1.8-8.3 mmO/L) • Creatinine: 75.98 (58-110)
ECG tracing: • Rate: 110 BPM • Presence of P wave • PR interval: <0. 20 secs. • QRS: <0.12 secs. • ABG result: • Ph: 7.33 (7.35-7.45) • PCO2: 34.5 mmHG ( 35-45 mmHG) • HC03: 20. 2 mEq/L (22-26 mEq/L
DIABETICKETOACIDOSIS • Diabetic ketoacidosis, or DKA, is a serious and possibly life-threatening condition that results from not having enough insulin characterized by hyperglycemia,ketonuria, acidocis and dehydration. • DKA is a medical emergency, and without treatment it can lead to death. DKA was first described in 1886; until the introduction of insulin therapy in the 1920s and was almost universally fatal.
DKA is most likely to occur in the early stage of type 1 diabetes before a diagnosis is made, during periods of sickness or when too little insulin is taken
The pancreas is about 6 inches long and sits across the back of the abdomen, behind the stomach. The head of the pancreas is on the right side of the abdomen and is connected to the duodenum (the first section of the small intestine) through a small tube called the pancreatic duct. The narrow end of the pancreas, called the tail, extends to the left side of the body. • The pancreas is a dual-function gland, having features of both endocrine and exocrine glands.
The part of the pancreas with endocrine function is made up of approximately a million] cell clusters called Islets of Langerhans. Four main cell types exist in the islets • α cells: secrete glucagon (increase glucose in blood), • β cells: secrete insulin (decrease glucose in blood), • Delta cells: secrete somatostatin (regulates/stops α and β cells), • Gamma cells:secrete pancreatic polypeptide. • The pancreas as an exocrine gland helps out the digestive system. It secretes pancreatic fluid that contains digestive enzymes that pass to the small intestine. These enzymes help to further break down the carbohydrates, proteins, and lipids (fats) in the chyme.
Decreased or absent insulin production Decreased or absent insulin production Increased blood glucose (Hyperglycemia) Fat metabolism • Osmotic Diuresis • Polyuria • Polydipsia • ketonuria Ketone bodies (Metabolic acidosis) Dehydration and electrolyte imbalance eg. hypotension • Compensatory Respiratory alkalosis) DKA
In various situations such as infection, insulin demands rise but are not matched by the failing pancreas. Blood sugars rise, dehydration ensues, and resistance to the normal effects of insulin increases further by way of a vicious circle. • Osmotic diuresis caused by hyperglycemia creates a shift in electrolytes with losses in potassium, sodium, phosphate and water.
ETIOLOGY • DKA most frequently occurs in those who already have diabetes, but it may also be the first presentation in someone who had not previously been known to be diabetic. • intercurrent illness (pneumonia, influenza, gastroenteritis, a urinary tract infection) • pregnancy, inadequate insulin administration • myocardial infarction (heart attack), stroke
Young patients with underlying eating disorder/ starvation, or may be using insufficient insulin for fear that it will cause weight gain. • Obesity, strong family history • Excessive alcohol intake/ use of cocaine • African, African-American and Hispanic people.
CLINICAL MANIFESTATIONS The symptoms of an episode of diabetic ketoacidosis usually evolve over the period of about 24 hours. • Nausea and vomiting • Excessive thirst. • Excessive urination • Abdominal pain that may be severe • Hyperglycemia
tachycardic (a fast heart rate) and low blood pressure may be observed. • "ketotic" odor is present, which is often described as "fruity", often compared to the smell of pear drops whose scent is a ketone. • Hyperventilation/ Kussmauls respiration • Fatigue
INTERVENTIONS/ TREATMENTS • Oxygen administration via non-rebreathing mask at 7 LPM. • Obtaining Vital Signs and blood sugar level. • Establishing peripheral IV access. • Obtaining Blood samples for laboratory investigations. • ABG sampling. • Fluid replacement (IVF NSS 1L).
Humulin R 10 units IV. • Obtaining ECG and Chest Xray. • Regular Insulin infusion ( IVF NSS 60 ML + Regular insulin 24 units at 15 ml/hr) • Premosan 10 MG IV. • Foleys catheterization. • Blood Glucose monitoring.
Implemented safety precautions (e.g. Siderails elevated). • Admission to Intensive care for close monitoring.
COMPLICATIONS • Cerebral edema • Low potassium (hypokalemia) • Hypovolemia • Death can occur without prompt management.
PHARMACOLOGY • Insulin is a peptide hormone, produced by beta cells of the pancreas, and is important for the utilization of glucose for cellular metabolism as well as proper metabolism of protein and fat.
SIDE EFFECTS OF INSULIN • Blurry vision. • Disturbed sensations. • Hypoglycemia • Allergic reaction. It can be moderate or even severe. Moderate symptoms include swelling, itchy or squeezing at injection place. Severe symptoms among other are: pulse become quickly, blood pressure descends, squeezing all over the body, breath become difficult. If a patient experiences the severe symptoms, he/she should immediately contact his/her doctor. ..
Lipodystrophy is a medical condition characterized by abnormal or degenerative conditions of the body's adipose tissue. ("Lipo" is Greek for "fat" and "dystrophy" is Greek for "abnormal or degenerative condition".) A more specific term, lipoatrophy is used when describing the loss of fat from one area.
PRIORITIZATION OF NURSING PROBLEMS • Fluid Volume deficit and Risk for Electrolyte imbalance • Impaired Breathing pattern • Risk for fall secondary to impaired neurologic function • Imbalanced Nutrition
NURSING HEALTH TEACHING • Never omit insulin dosage. Take the usual dosage of insulin as prescribed. Compliance of medication regimen is significant. • Monitor blood glucose every 2-4 hours. Record test results. • Drink plenty of fluids 6-8 oz of water every hour is recommended. • If unable to eat, drink fluids that contain carbohydrates such as fruit juices, regular soda. • Seek health care provider if illness becomes severe or unmanageable
Rotate injection sites for insulin administration to prevent muscle atrophy. • Inspect the feet carefully and daily for calluses, corns, blisters, abrasions, redness and nail abnormalities • Prevent moisture between toes to prevent maceration of the skin. • Wear well fitting non compressive shoes.
CONCLUSION It is to significant to determine DKA as early as possible for emergent intervention. DKA is a life threatening condition but with early detection the better the prognosis. Nurses play a vital role in managing or preventing DKA. Patients who are at risk for developing DKA can also do their part by complying with their medication regimen, avoiding alcohol, and knowing the manifestations that need prompt treatment. Managing DKA is a multidisciplinary approach from Physician, Nurses and other healthcare staff.
REFERENCES • http://en.wikipedia.org/wiki/Diabetic_ketoacidosis • Mosby’s Comprehensive Review of NCLEX-RN Examination 19th Edition • Saunder’s NCLEX-RN review 9th Edition • Lippincott Manual of Nursing Practice 9th Edition