nursing process - Nursing Case Study

Pathophysiology

Topic: Diabetes Mellitus

• Primary mechanism: Chronic hyperglycemia due to insulin resistance or deficiency. In type 1, the pancreas fails to produce insulin. In type 2, the body becomes resistant to insulin or doesn't produce enough.

• Secondary mechanism: High blood sugar levels lead to glycosylation of various tissues, causing complications like retinopathy, neuropathy, and nephropathy.

• Key complication: Hyperglycemic emergencies like diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) can occur, characterized by extreme elevations in blood glucose levels, dehydration, and altered consciousness.

Patient Profile

Demographics:

56-year-old, male, factory worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes, Smoker for 30 years

• Current medications: Metformin, Lisinopril, Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Chest pain and shortness of breath

• Key symptoms: Mild chest discomfort, fatigue, sweating, dizziness, intermittent shortness of breath

• Vital signs: Blood pressure 145/95 mmHg, pulse 90 bpm, respiration rate 24 breaths per minute, temperature 98.6 degrees Fahrenheit, oxygen saturation 92% on room air.

Section 1

New Diagnostic Results:

The patient's blood glucose level was significantly elevated at 450 mg/dL, and his HbA1c was 9.8%, indicating poor blood sugar control over the past three months. His EKG showed ST-segment elevations in leads II, III, and aVF, hinting at an inferior wall myocardial infarction (MI), a condition often associated with Type 2 diabetes due to the increased risk of atherosclerosis. The Troponin T level was also elevated at 0.5 ng/mL, further supporting the diagnosis of an MI.

Change in Patient Status:

The patient started complaining of worsening chest pain, which he described as a "heavy pressure." His blood pressure increased to 160/100 mmHg, pulse rate was 100 bpm, and his oxygen saturation dropped to 88% on room air. He appeared visibly anxious, was profusely sweating, and his skin was cool and pale. His respiration rate increased to 30 breaths per minute, suggesting possible respiratory compensation for metabolic acidosis, which could be a result of his elevated blood glucose levels. These changes in his condition along with his elevated blood glucose level indicate possible hyperglycemic hyperosmolar state (HHS), a serious complication of Type 2 diabetes.

Section 2

Change in Patient Status:

Despite initial interventions, the patient's condition continued to worsen. His blood pressure spiked to 175/110 mmHg and his heart rate increased to 120 bpm, indicating a worsening cardiovascular status. His oxygen saturation further dropped to 82% on room air, suggesting deteriorating respiratory function. The patient's consciousness level started to decrease, with a Glasgow Coma Scale score dropping to 11/15. The patient also showed signs of dehydration, including dry mucus membranes and poor skin turgor. His blood glucose level remained elevated at 500 mg/dL, suggesting that his body was unable to adequately utilize the insulin he was receiving.

Response to Interventions:

Despite receiving IV fluids and insulin, the patient's blood glucose levels remained dangerously high, and his symptoms of chest pain and breathlessness showed no signs of improvement. In response, the medical team decided to increase the insulin dosage and supplemented his treatment with oxygen therapy to help improve his oxygen saturation levels. The team also administered nitroglycerin to help alleviate his chest pain and reduce myocardial oxygen demand. Despite these interventions, his condition remained critical and he was transferred to the Intensive Care Unit for closer monitoring and further treatment.

Section 3

New Diagnostic Results:

Despite the aggressive interventions, the patient's blood glucose levels continued to fluctuate, remaining dangerously high at 450 mg/dL. A repeat EKG showed new ST segment elevations in multiple leads, suggesting an evolving myocardial infarction. Laboratory results also showed a significant increase in cardiac enzymes, including a troponin level of 4.5 ng/mL (normal range: 0.00-0.04 ng/mL), further supporting the diagnosis of an acute myocardial infarction.

In addition, his arterial blood gas (ABG) analysis revealed a pH of 7.25 (normal range: 7.35-7.45), a PaCO2 of 50 mmHg (normal range: 35-45 mmHg), and a bicarbonate level of 18 mEq/L (normal range: 22-28 mEq/L), suggesting a combined metabolic and respiratory acidosis. This could be attributed to poor tissue perfusion and oxygenation secondary to the myocardial infarction and exacerbated by poor glucose control.

The patient's elevated blood urea nitrogen (BUN) at 45 mg/dL and creatinine at 2.8 mg/dL indicated a worsening renal function, likely related to dehydration and poor perfusion. His serum potassium was also elevated at 5.5 mEq/L, which could be a result of renal impairment and acidosis, and posed a risk for further cardiac complications. These new findings necessitated a reevaluation of the patient's treatment plan and further interventions.

Section 4

Change in Patient Status:

Over the next few hours, the patient's status began to deteriorate. His blood pressure dropped to 90/60 mmHg, heart rate increased to 110 bpm, and his oxygen saturation levels dropped to 88% on room air. His skin was cool and clammy, and he started complaining of increased chest pain, rated an 8 on a 10-point scale. His respiratory rate increased to 26 breaths per minute, with shallow respirations, indicating possible respiratory distress. This acute change in status suggested a worsening of the myocardial infarction and a possible onset of cardiogenic shock, exacerbated by the underlying metabolic and respiratory acidosis.

On reassessment, lung sounds revealed crackles in the lower lobes bilaterally, suggesting fluid overload or impending heart failure. His abdomen was distended with decreased bowel sounds, likely a result of decreased perfusion and possible ileus. His urine output also decreased to less than 30 mL/hour, indicating worsening renal function. The patient's Glasgow Coma Scale (GCS) score dropped to 12 from a previous 15, which indicated a diminishing level of consciousness and potential neurological compromise. These alarming changes necessitate immediate intervention to stabilize the patient and prevent further deterioration.

Section 5

New Diagnostic Results:

The results from the patient's latest blood tests have started to come in, and they are not favourable. His troponin levels have risen sharply, indicating increased heart muscle damage. His BNP (B-type natriuretic peptide) level is over 900 pg/mL, suggesting heart failure. His creatinine level has also increased to 2.1 mg/dL, indicating that his kidneys are struggling, likely due to reduced blood flow. His blood gases show a worsening metabolic acidosis, with a pH of 7.28, bicarbonate level of 18 mmol/L, and a partial pressure of carbon dioxide (PaCO2) of 38 mmHg, which is likely contributing to his respiratory distress.

The EKG is showing a new onset of ST-segment elevation, which is a clear sign of ongoing myocardial infarction. This is consistent with his increased chest pain and unstable vital signs. The chest X-ray also revealed bilateral lower lobe infiltrates, which could be due to congestive heart failure or acute respiratory distress syndrome secondary to shock. The combination of these new diagnostic results and the patient's declining status underscores the need for immediate and aggressive intervention. The team will need to consider a range of potential treatments, including medications, possible surgical interventions, and supportive measures such as oxygen therapy and potential intubation. The upcoming decisions will require careful clinical reasoning, weighing the risks and benefits of each option in light of the patient's rapidly changing condition.