GTNIMohamed ELBadrawy Ragab

Date:7\5\2015.

Under supervision:

Mrs. Omnia Helaly

Points to cover

Patient data. Medical diagnosis. Diagnostic &lab results. Medications. Psychosocial. Nursing care plan. Preventing complications. Research questions.

The Aim Effective critical care. Connect between theory and practice. Simple nursing care have great outcome. Critical thinking.

Patient summary patient’s initials: RL, 42 years male. From

Nmsa. admission date 12-3-2015. allergies: NKA admitting diagnosis: atrial fibrillation and diabetic ketoacidosis. past medical history: Hernia. current vital signs: Pulse is 82, Bp 110\70 mmHg, temp 37.2 and Spo2 100%.

Patient journey

Ambulance

Emergency

ICU

CCU

Medical diagnosis

Medical diagnosis: diabetic ketoacidois (DKA )and atrial fibrillation ?

Diabetic ketoacidosis Pathophysiology: (DKA) is caused by a profound

deficiency of insulin and is characterized by hyperglycemia, ketosis, in conditions of severe illness or stress when the pancreas cannot meet the extra demand for insulin.

(Lewis 2014.)

Etiology Change in diet and exercise regimen. Undiagnosed diabetes mellitus Inadequate treatment of existing diabetes

mellitus Insulin not taken as prescribed Infection

(Lewis 2014.)

1-lethargy and

weakness.

2dry mouth.

3. Thirst .

4. Abdominal

pain.

5. Nausea and

vomiting.

6. confusion.

7. Flushed skin.

8-Sunken eyes

11- Labored breathing (Kussmaul respirations)10- Breath odor of ketones

12- Glucosuria and ketonuria)

9- Serum glucose >250

Clinical manifestation

(Lewis 2014.)

Atrial fibrillation Pathophysiology:

Total disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction

(Lewis 2014.)

Etiology Fluid Electrolyte disturbance. Alcohol intoxication. Caffeine use. Stress. Cardiac surgery.

(Lewis 2014.)

1-Palpitation

s.2-

Weakness, Reduced ability to exercise

3-Fatigue

4-Lightheade

dness5-Dizziness

6-Confusion

6-Shortness of breath and chest

pain

Clinical manifestations

(Lewis 2014.)

Nursing care First ABCD: Maintain patent air way. Administer O2 via nasal canula or non re-breathing

mask. Assess respiratory rate and lung sound. Administration of IV fluids. Assessment of mental status. Electrolyte replacement. The main goal of treatment is to maintain adequate

cardiac output and tissue perfusion. Cardiac assessment. ECG monitoring.

(Lewis 2014.)

2 abnormal lab values and diagnostic tests.

ECG. Blood Glucose level.

Atrial fibrillation

First

ECG: Atrial fibrillation: ECG

Characteristics. atrial rate may be as high as 350 to 600 beats/minute.

P waves are replaced by chaotic, fibrillatory waves.

ventricular rate is between 60 and 100 beats/minute usually irregular.

(Lewis 2014.)

Blood glucose 1221 MG\dl. Hyperglycemia. pancreas cannot meet the extra

demand for insulin. When the circulating supply of insulin

is insufficient, glucose cannot be properly used for energy. The body compensates by breaking down fat stores as a secondary source of fuel (ketones).

(Lewis 2014.)

2 main medications.

•Insulin.•Cordarone.

INSULINS (rapid acting)antidiabetics, hormones

G\T nameClassification

Control of hyperglycemia in patients with type 1 or type 2 diabetes mellitus.

Indications

stimulating glucose uptake in skeletal muscle and fat, inhibiting hepatic glucose production.

Action

Hypoglycemia, erythema, lipodystrophy, pruritis, swelling. Allergic reaction.

Side effect

erythema, lipodystrophy, pruritis, swelling, Corticosteroids, thyroid supplements, estrogens. Hypoglycemia.

Contraindicati-ons. interaction

generally 0.5–1 unit/kg/day. Dose

Subcutaneous. Route

hypoglycemia (anxiety; restlessness; tingling in hands, feet, lips, or tongue.Assess patient for signs of allergic reactions (rash, shortness of breath, wheezing, rapid pulse, sweating, low blood pressure) during therapy.Monitor blood glucose.

Nursing assessemnt

Cordarone \ amiodarone Antiarrhythmics.

G\T nameClassification

Life-threatening ventricular arrhythmias. Indications

Prolongs action potential and refractory period. Inhibits adrenergic stimulation. Slows the sinus rate, increases PR and QT intervals, and decreases peripheral vascular resistance (vasodilation).

Action

Respiratory distress syndrome, confusional states, disorientation, hallucinations, dizziness, fatigue, malaise, headache, insomnia.

Side effect

Patients with cardiogenic shock; Severe sinus node dysfunction; 2nd- and 3rd-degree AV block.↑ levels of digoxin, beta blockers, calcium channel blockers.

Contraindicati-ons. interaction

10 mg/kg/day. Dose

PO. Route

Monitor ECG continuously. Assess ARDS.Assess for signs of pulmonary toxicity (rales/crackles, decreased breath sounds, pleuritic friction rub, fatigue, dyspnea, cough, wheezing, pleuritic pain, fever, hemoptysis, hypoxia).

Nursing assessment

2 cultural, spiritual, and psychosocial concerns

Patient have no religion. Patient feel lonely. He is not married. He have insurance.

communication

With the patient I used: broad opening :”what do you want to talk about”

With the patient I used: Summarizing :

“we disused…”.

Educational needs Read about the new disease. Nutrition intake for diabetic person. Body care. Insulin injections.

Nursing diagnosis

nursing diagnosis.1. Acute pain: Related to disease affect on the CNS

as evidenced by patient was moaning and he feel pain .

2. Risk for decreased cardiac output: RT Altered electrical conduction. Reduced myocardial contractility.

3. Imbalanced blood glucose level: related to Insulin deficiency—decreased uptake or utilization of glucose by the tissues resulting in increased protein and fat metabolism. as evidenced by increased the blood glucose level.

(Sparks,2014.)

Expected outcomes Acute pain: Patient verbalizes adequate relief of pain or

ability to cope with incompletely relieved pain. Risk for decreased cardiac output : Maintain or achieve adequate cardiac output

as evidenced by BP and pulse within normal range, adequate urinary output, palpable pulses of equal quality, and usual level of mentation.

Imbalanced blood glucose level: Maintain glucose in normal range.

(Sparks,2014.)

Interventions Acute pain: Assess pain characteristics.

Assess for probable cause of pain.

Administer pain medication. (Pethidine 50 Mg)

(Sparks,2014.)

Risk for decreased cardiac output.

Palpate pulses, noting rate, regularity, amplitude (full or thready), and symmetry. Document presence of pulse deficit.

Auscultate heart sounds, noting rate, rhythm, presence of extra heartbeats, and dropped beats.

Determine type of dysrhythmia and document with rhythm strip if cardiac or telemetry monitoring.

(Sparks,2014.)

Review type(s) of insulin used.

Observe for signs of hypoglycemia—changes in LOC, cool and clammy skin, rapid pulse, hunger, irritability, anxiety, headache, lightheadedness, and shakiness.

Monitor laboratory studies, such as serum glucose, acetone, pH, and HCO3

.

Imbalanced blood glucose

(Sparks,2014.)

EvaluationAcute pain:Met, patient bcame more comfort and relived of

moaning sound.

Risk for decreased cardiac output:Met, achieve adequate cardiac output as

evidenced by BP and pulse within normal range, adequate urinary output.

Imbalanced blood glucose:Met, patient has decreased blood glucose level.  (Sparks,2014.)

Concept map

concerns reported to the RN. Neurologic, patient is confused

(safety). ECG atrial fibrillation (cardiac

output). Patient blood glucose decreased

very fsat.

Discharge Instructions: Follow up. Best Nutrition. Body care. Medication. Injection.

(Kornusky,2014.(

At home. 1. Continue prescribed diabetic medications .2. Report a glucose reading > 300 mg/dL or urine

ketones to the treating clinician3. If nauseous, eat frequent (e.g., 6–8times a day),

small meals of soft foods such as gelatin, soup, custard, or crackers

4. If vomiting, diarrhea, or fever persists, continue calorie intake through liquids (e.g., orange juice, broth, or Gatorade) every 30–60minutes

5. Report nausea, emesis, or diarrhea promptly to the treating clinician

6. If unable to keep liquids down, hospitalization may be necessary to prevent DKA

(Kornusky,2014(.

Handouts & leaflets Diabetic food pyramids. Diabetic nutrition. Insulin injection technique.

(Kornusky,2014(.

Preventing Complications: What are you alert for in this patient?

hypoglycemia, fluid and electrolyte imbalance, cardiac embolism , non compliance. And hyperglycemia.

2. What are the important assessments to make blood glucose monitoring, ECG.

3. What complications may occur? Complications of DKA include electrolyte imbalances, cerebral edema, thrombotic events(e.g., pulmonary embolism, stroke,deep vein thrombosis), and acute renal failure

4. What interventions will prevent complications? monitor blood glucose level, administer anti coagulant thereby and anti arrhythmic drugs, ECG monitoring.

5. What will you do if complications do occur?ABCD, need mobilization from the team.

Research question Is there any relation between atrial

fibrillation and DKA?

How can DKA cause fluid and electrolyte disturbance?

Answer DKA cause metabolic acidosis that

lead to increased concentration of hydrogen ions (H+) or decreased concentration of bicarbonate (HCO3–).

In which make potassium shift from intracellular to extracellular.

When potassium decreased from cardiac cells it effect on the conduction system which results in arrhythmia(atrial fibrillation). (Kornusky,2014(

.

Answer the kidneys also excrete water and

electrolytes, leading to dehydration and electrolyte imbalances.

Electrolyte imbalances and hyperosmolarity (i.e., increased solution concentration expressed as osmoles of solute/kg of serum water) can result in cardiac arrhythmias and even coma. (Adler,2013.(

Reference Kornusky, J. 2014. Metabolic Acidosis. Cinahl

Information Systems. Vol1.Pag 1-3.

Adler,A. Cabrera,G. 2013. Diabetic Ketoacidosis in Adults. Pag1-4.

MYOJO, T. 2012. Recurrent Ventricular Fibrillation Related to Hypokalemia in Early Repolarization Syndrome. Wiley Periodicals, Vol 35. pag 1-4.

Reference Con’d

Lewis S, Dirksen S, Heitkemper M, Bucher L, Camera I (2013) Medical-Surgical Nursing: Assessment and Management of Clinical Problems (8th ed) p1218-1253 St. Louis Elsevier Mosby