PRESSURE ULCER - Nursing Case Study

Pathophysiology

• Primary mechanism: Pressure ulcers, also known as bedsores, are primarily caused by sustained pressure on a specific area of the body, particularly where the bone is close to the skin (like hips, heels, and tailbone). The pressure limits blood flow to these areas, depriving tissues of oxygen and nutrients needed for cell health and survival, leading to cell death and ulcer formation.

• Secondary mechanism: Friction and shear also contribute to pressure ulcer development. Friction can damage the top layer of skin, making it more vulnerable to pressure. Shear occurs when skin moves one way and the underlying bone moves in another, stretching and possibly tearing blood vessels, impairing blood flow.

• Key complication: If left untreated, pressure ulcers can lead to serious infections, including cellulitis (skin and tissue infection) or osteomyelitis (bone infection). These infections can further exacerbate tissue damage and potentially lead to sepsis, a life-threatening condition.

Patient Profile

Demographics:

68-year-old male, retired firefighter

History:

• Key past medical history: Diabetes mellitus type II, hypertension, former smoker, and a history of stroke 5 years ago that caused limited mobility on his left side

• Current medications: Metformin, Lisinopril, Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Painful swelling and redness on sacral area

• Key symptoms: Patient complains of localized pain and reports feeling feverish. Upon inspection, a stage II pressure ulcer was found on the sacral area, with redness, swelling, and some draining pus. The patient has limited mobility, which has led to prolonged pressure on the sacral area.

• Vital signs: Blood pressure 140/90 mmHg, Pulse 88 bpm, Respiratory rate 18 breaths per minute, Temperature 38.3°C (101°F), Oxygen saturation 95% on room air.

Section 1

Change in patient status:

Over the next 24 hours, the patient's condition worsens. His temperature increases to 38.9°C (102°F), and his blood pressure drops to 125/70 mmHg. Despite receiving intravenous antibiotics, the patient's pain in the sacral area intensifies. On examination, the pressure ulcer appears to have deepened, with increased pus drainage and a foul odor indicative of necrotic tissue.

New complications:

The patient's worsening condition and signs of systemic infection raise concerns about possible sepsis, which is a life-threatening response to infection. Laboratory blood tests reveal a significant rise in white blood cell count (17,000 cells/mm3), indicating an ongoing infection. Additionally, his blood glucose levels are elevated at 250 mg/dL, despite his regular metformin regimen, suggesting that the stress of the infection is adversely affecting his diabetes management. The patient also begins to show signs of confusion and disorientation, which may be due to sepsis or possibly a high blood sugar level. The increasing depth of the pressure ulcer also suggests possible osteomyelitis, a bone infection that would require prompt and aggressive treatment.

Section 2

Change in patient status:

Over the next few hours, the patient's condition continues to deteriorate. His temperature spikes to 39.5°C (103.1°F), and his blood pressure further drops to 110/65 mmHg. His level of consciousness decreases, and he becomes lethargic, responding only to painful stimuli. His breathing becomes shallow and rapid, with a rate of 28 breaths/min. He also begins to complain of increased pain in the sacral area, with a severity rating of 8 on a scale of 1 to 10, despite the administration of pain medication.

New complications:

The patient's clinical presentation and ongoing signs of systemic infection continue to suggest possible sepsis. Repeat laboratory tests show an increase in his white blood cell count to 20,000 cells/mm3, further confirming the presence of an uncontrolled infection. His blood glucose levels remain high at 280 mg/dL, despite the administration of insulin. A new finding on the blood gas analysis shows a metabolic acidosis, with a bicarbonate level of 18 mEq/L and a pH of 7.30, possibly indicating an uncontrolled diabetic ketoacidosis or septic shock. The patient's worsening mental status, combined with his deteriorating vital signs and laboratory results, signal a critical condition that needs immediate intervention and re-evaluation of current treatment strategies.

Section 3

Change in patient status:

As the night progresses, the patient's breathing becomes more labored, with an increased respiratory rate of 35 breaths/min. His blood pressure continues to drop, now measuring at 100/60 mmHg. The patient becomes increasingly unresponsive, only responding to painful stimuli. His skin is pale and cool to touch, and his peripheries are mottled. His pulse oximetry reading drops to 90%, indicating possible hypoxemia.

Initial assessment findings:

The nurse conducts a thorough physical examination of the patient. His sacral pressure ulcer appears to have increased in size, with a foul-smelling discharge noted. The surrounding skin is warm and erythematous. Upon auscultation, the nurse notes decreased breath sounds in the lower lobes bilaterally, indicating possible pneumonia. The Glasgow Coma Scale is reassessed and shows a decrease from 15 to 11, signaling a significant decrease in the patient's level of consciousness.

New diagnostic results:

The healthcare team decides to repeat the sepsis panel, which now shows an elevated procalcitonin level of 8 ng/mL, further supporting the suspicion of sepsis. The arterial blood gas analysis reveals a worsening metabolic acidosis, with a pH of 7.25 and a bicarbonate level of 16 mEq/L. The blood glucose level remains high, now at 300 mg/dL, despite continuous insulin administration. The urinalysis report shows the presence of ketones, suggesting uncontrolled diabetes and possible diabetic ketoacidosis. These findings, along with the patient's deteriorating clinical status, necessitate a rapid reassessment of the patient's treatment plan to prevent further complications.

Section 4

Change in patient status:

Despite aggressive fluid resuscitation and antibiotic administration, the patient's condition continues to deteriorate. His blood pressure drops further to 90/50 mmHg, and his heart rate increases to 120 beats/min, suggesting a state of shock. The patient's respiratory rate escalates to 40 breaths/min and he appears increasingly distressed. His pulse oximetry reading falls to 85%, despite supplemental oxygen being administered through a non-rebreather mask. He is now minimally responsive, even to painful stimuli, and his Glasgow Coma Scale drops to 8.

Response to interventions:

Despite the healthcare team's best efforts, the patient's sacral pressure ulcer continues to worsen, with increased purulent discharge and surrounding tissue necrosis noted. The wound dressing changes and topical antibiotics appear to be having little effect, suggesting a possible resistant bacterial infection. Given the patient's deteriorating respiratory status, a decision is made to intubate and mechanically ventilate the patient to ensure adequate oxygenation. Insulin infusion is increased to manage the persistently high blood glucose levels, and the patient is started on a bicarbonate infusion to counteract the metabolic acidosis.

The deteriorating clinical picture, refractory hypotension, and the lack of response to interventions suggest a severe sepsis progressing to septic shock, warranting immediate escalation of care. The healthcare team is now faced with the challenge of managing the patient's septic shock, uncontrolled diabetes, and a worsening pressure ulcer, all while trying to identify the source of infection and appropriate antibiotic therapy.

Section 5

New diagnostic results:

The results of the patient's blood cultures reveal the presence of Methicillin-resistant Staphylococcus aureus (MRSA), a highly resistant bacterium, explaining the lack of response to the current antibiotic regimen. Lab results also show an increased white blood cell count of 18,000/uL, further indicating an ongoing systemic infection. Blood gas analysis reveals a pH of 7.28, a PaCO2 of 40 mmHg, bicarbonate of 18 mEq/L, and a base excess of -5 mEq/L, indicating a persistent metabolic acidosis. The patient's blood glucose levels remain elevated at 300 mg/dL despite the increased insulin infusion.

New complications:

During the nurse's routine assessment, it is noticed that the patient's lower extremities are cold and mottled, with weak peripheral pulses. His capillary refill time is greater than 3 seconds. The patient's urine output has also decreased to less than 20 mL/hr over the past 6 hours, suggesting possible acute kidney injury. A bedside ultrasound confirms the suspicion of decreased renal perfusion. These findings indicate that the septic shock may be leading to multi-organ dysfunction syndrome, a severe complication with high mortality rates. The healthcare team must urgently revise their management plan to address these new complications, while continuing to manage the patient's septic shock, uncontrolled diabetes, and worsening pressure ulcer.