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Prepared by: Tristan Villanueva Arcibal BSN-RN Presented on: July 16, 2013 A CASE PRESENTATION OF A PATIENT WITH DIABETIC KETOACIDOCIS (DKA)

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Presentation on theme: "Prepared by: Tristan Villanueva Arcibal BSN-RN Presented on: July 16, 2013 A CASE PRESENTATION OF A PATIENT WITH DIABETIC KETOACIDOCIS (DKA)"— Presentation transcript:

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2 Prepared by: Tristan Villanueva Arcibal BSN-RN Presented on: July 16, 2013 A CASE PRESENTATION OF A PATIENT WITH DIABETIC KETOACIDOCIS (DKA)

3  DEMOGRAPHIC DATA Name: Mr. X Case no. : Age: 28 y/o Gender: Male Nationality: Saudi Admission date: Time of arrival: 0840H Chief complaints: Persistent vomiting,Low blood pressure, High blood glucose, Altered mental status Diagnosis: DKA

4  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

5  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

6  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

7  EXTREMITIES  Limbs are normal  (-) weakness, contractures, joint swelling/ paralysis

8  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.

9  SLIDING SCALE Blood Glucose (mg/dl)Insulin dose (SC) UNITS UNITS UNITS UNITS UNITS More than 400Seek medical intervention

10  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.

11  Laboratory tests: Glucose (random): 23.4 mmo/L ( mmo/L) Urinalysis : ++ketones CBC WBC: 9.04 ( ) HGB: 14.3 ( ) HCT: 39.6 ( ) PLT: 350 ( )  Electrolytes: NA+: 141 mmO/L ( mmO/L) K+: 4.3 mmO/L ( mmO/L) Cl+ :98 mmO/L ( mmO/L)  BUN: 4.42 mmO/L ( mmO/L)  Creatinine: (58-110)

12  ECG tracing: Rate: 110 BPM Presence of P wave PR interval: <0. 20 secs. QRS: <0.12 secs.  ABG result: Ph: 7.33 ( ) PCO2: 34.5 mmHG ( mmHG) HC03: mEq/L (22-26 mEq/L

13  DIABETIC KETOACIDOSIS  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.

14  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

15  ANATOMY AND PHYSIOLOGY OF THE PANCREAS

16  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.

17  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.

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19 Decreased or absent insulin production Dehydration and electrolyte imbalance eg. hypotension Osmotic Diuresis Polyuria Polydipsia ketonuria Osmotic Diuresis Polyuria Polydipsia ketonuria Ketone bodies (Metabolic acidosis) Ketone bodies (Metabolic acidosis) Fat metabolism Compensatory Respiratory alkalosis) Increased blood glucose (Hyperglycemia) Increased blood glucose (Hyperglycemia) DKA

20  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.

21  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

22  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.

23  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

24  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

25  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).

26  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.

27  Implemented safety precautions (e.g. Siderails elevated).  Admission to Intensive care for close monitoring.

28  COMPLICATIONS  Cerebral edema  Low potassium (hypokalemia)  Hypovolemia  Death can occur without prompt management.

29  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.

30  TYPES OF INSULIN Types of Insulin preparations OnsetPeakDuration Regular Insulin ( Humulin R, Novolin R) Within 30 minutes 1-3 hours6-8 hours NPH Insulin (Novolin N, Humulin N) 2 hours4-12 hours18-26 hours

31  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...

32 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.

33  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

34  NURSING CARE PLAN AssessmentNsg. Diagnosis PlanNursing Implementation RationaleEvaluation Subjective “Ana ibga moya” as verbalized by the patient. Objective Persistent vomiting, Poor skin turgor Excessive urination and thirst, dry oral mucosa. BP= 90/60 mmHg PR= 110 BPM GRBS= 450 Fluid Volume deficit and Risk for Eletrolyte imbalance related to osmotic diuresis secondary to uncontrolled blood glucose.  To be able to correct patient’s fluid volume loss, maintain Electrolyte levels and to lower the blood glucose level from 450 mg/dl to 250 mg/dl or less within 1 to 2 hour of nursing care as evidenced by:  Return of Vital Signs to normal levels BP=120/80 mmHG PR= BPM Monitored Vital signs and blood glucose level Administered Intravenous Fluid as ordered (e.g.IVF NSS 1-2 L Regular Insulin IV administration as prescribed (e.g. Regular Insulin 10 units IV Obtained blood sample and ABG To determine patient’s status. To replace fluid loss and maintain electrolyte level. To decrease or correct hyperglycemia. to determine severity of dehydration, eletrolyte and acid-base imbalance. Goal was patient met. Patient was rehydrated, within 1 hour of care. BP=120/70 mmHG PR= 89 BPM GRBS= 250 mg/dl. No vomiting.

35 AssessmentNsg. Diagnosis PlanNsg. Intervention RationaleEvaluation  Eletrolyte levels within normal range e.g serum potassium mEq/L  No signs of dehydration such as return of normal skin turgor.  Absence of vomiting  Foleys catheterization  Administered antiemetic drugs as ordered e.g. Premosan 10 mg IV To monitor urine output. To control nausea and persistent vomiting.

36 AssessmentNsg. Diagnosis PlanNursing Implementation RationaleEvaluation Subjective N/A Objective Restlessness Mild cyanosis Nasal flaring Increased antero- posterior diameter Shortness of breath Impaired breathing pattern related to acid base imbalance secondary to uncontrolled hyperglycemia  After 1-2 hours of nursing care and management, patient will be able to:  Achieve maximum lung expansion w/ adequate ventilations.  Report feeling of comfortable breathing Assessed respiratory rate, depth and oxygenation Administered oxygen inhalation as ordered e.g. NRM 10 LPM Elevated head of bed to fowlers position Administered Regular Insulin 10 units IV as ordered to detect early signs of respiratory compromise. to support oxygenation. To facilitate lung expansion and ease in DOB. To treat hyperglycemia Goal partially met, patient was able to achieve adequate oxygenation as evidenced by :  Return of normal breathing pattern  Respiratory rate of 18 bpm  Return of normal skin color

37 AssessmentNsg. Diagnosis PlanNsg. Implementation RationaleEvauation ABG- Ph: 7.33 PCO2: 34.5 mmHG HC03: mEq/L RR= 30 breaths per minute  Achieve a respiratory rate of breaths per minute.

38  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

39  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.

40  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.

41  REFERENCES Mosby’s Comprehensive Review of NCLEX-RN Examination 19 th Edition Saunder’s NCLEX-RN review 9 th Edition Lippincott Manual of Nursing Practice 9 th Edition

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