DEEP TISSUE INJURY - Nursing Case Study

Pathophysiology

• Primary mechanism: Prolonged pressure and shear forces on the skin, predominantly over bony prominences, result in tissue ischemia. This is due to obstruction of blood flow leading to hypoxia and nutrient deprivation in deep tissues, causing cell death and tissue necrosis.

• Secondary mechanism: Reactive hyperemia, a protective response that increases blood flow to the affected area, could be impaired under constant pressure. This exacerbates ischemia and contributes to the development of deep tissue injury.

• Key complication: Disruption of the skin and underlying tissues can serve as an entry point for bacteria, leading to infection. Severe cases can progress to sepsis if not treated promptly.

Patient Profile

Demographics:

54-year-old male, construction worker

History:

• Key past medical history: Hypertension, Type II Diabetes, previous deep tissue injuries due to accidents at work

• Current medications: Metformin, Lisinopril

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Unbearable pain in left leg, difficulty walking

• Key symptoms: Swelling and warmth in the leg, skin discoloration, fever

• Vital signs: Blood pressure 160/95 mmHg, pulse rate 105 bpm, temperature 38.6°C, respiratory rate 22 breaths per minute, oxygen saturation 93% on room air

Section 1

Initial Assessment Findings:

On physical examination, the patient's left leg was found to be markedly swollen and erythematous with localized heat. There was also evidence of blanching and purpura on the surface of the skin. The patient reported a pain rating of 8 out of 10 on the Numeric Rating Scale (NRS). His capillary refill time was determined to be greater than 3 seconds which suggested impaired peripheral circulation. On palpation, the tissue surrounding the affected area felt hard and tough, indicative of potential deep tissue injury.

The patient's vital signs were recorded again, showing a blood pressure of 165/100 mmHg, pulse rate of 110 bpm, temperature of 39.1°C, and respiratory rate increasing to 25 breaths per minute. His oxygen saturation had dropped slightly to 91% on room air. Given the patient's history and current symptoms, the preliminary diagnosis was deep tissue injury with a possible underlying infection. This raised concerns about the risk of sepsis given his elevated temperature and increased heart rate, which are signs of systemic inflammatory response. The medical team decided to initiate antibiotic therapy and requested for further laboratory tests and imaging studies to confirm the diagnosis and assess the extent of the injury.

Section 2

Following the initial assessment, the laboratory results of the patient's blood sample indicated a high white blood cell (WBC) count of 21,000 cells/mm3, which is significantly elevated from the normal range of 4,500-11,000 cells/mm3. This finding corroborated the clinical suspicion of a systemic infection. Moreover, the results of the C-reactive protein (CRP) test were equally alarming, with a value of 150 mg/L, far above the standard range of 0-10 mg/L. This marker's elevated level further indicated severe inflammation in the body, potentially due to infection. The patient's blood cultures were sent to the lab to identify the causative organism of the infection.

Imaging studies, including an ultrasound of the affected leg, were performed. The ultrasound revealed a hypoechoic area with irregular margins deep in the tissues of the leg, confirming a deep tissue injury. Moreover, the Doppler study of the lower limb vessels suggested reduced blood flow to the affected area, indicating possible vascular compromise due to the swelling and inflammation. The patient's clinical status seemed to be deteriorating, with his pain level escalating to a 9 on the NRS scale despite analgesic administration. The medical team was faced with the challenge of managing an escalating infection, possible sepsis, and ensuring adequate blood flow to the affected tissues to prevent further tissue necrosis.

Section 3

The patient's condition worsened over the next few hours. He became febrile with a temperature of 38.5°C, his heart rate increased to 120 beats per minute, and his blood pressure fell to 90/60 mmHg. Notably, an increased respiratory rate of 24 breaths per minute was observed. His oxygen saturation also dropped to 92%, despite supplemental oxygen. These changes suggested the development of systemic inflammatory response syndrome (SIRS), a precursor to sepsis. The patient started to appear confused, indicating a possible decrease in his perfusion status due to the systemic infection.

The blood culture results came back positive for Staphylococcus aureus, a common causative organism for skin and soft tissue infections. Given the patient's deteriorating condition, the medical team decided to initiate aggressive treatment for sepsis. Intravenous antibiotics were started, specifically Vancomycin, which is often used for severe Staphylococcus aureus infections. Fluid resuscitation was also initiated to counteract his hypotension and maintain tissue perfusion. The patient's response to these interventions will be critical in determining the course of his condition. The team will need to closely monitor his vital signs, repeat lab values, and assess his level of consciousness to gauge his response to treatment. The worsening of the patient's condition underscores the need for swift and decisive action to curb the spread of the infection and reduce further tissue damage.

Section 4

Despite aggressive treatment, the patient's condition continued to decline. His temperature increased to 39.3°C, his heart rate rose to 130 beats per minute, and his blood pressure further dropped to 85/55 mmHg. His respiratory rate also climbed to 28 breaths per minute and his oxygen saturation fell to 88%, even with increased supplemental oxygen. The patient's confusion worsened, and he became increasingly lethargic. His urine output also decreased to 20 ml/hr, suggesting possible acute kidney injury secondary to sepsis.

New lab results showed a rise in the patient's white blood cell count to 18,000 cells/mm³, indicating ongoing infection. His lactate level was also high at 4 mmol/L, indicating tissue hypoperfusion. Creatinine level was elevated at 1.8 mg/dL, and his blood urea nitrogen (BUN) was 30 mg/dL, both suggesting impaired renal function. The medical team decided to consult the critical care team given the patient's deteriorating condition and the development of sepsis-induced organ dysfunction. These findings highlight the seriousness of the patient's condition and the need for escalated care. As the patient's status continues to worsen, the medical team will need to reassess their plan of care and consider more aggressive interventions.

Section 5

Upon reassessment, the patient's condition furthered worsened. He developed a new onset of severe abdominal pain, and his abdomen was distended and rigid on physical examination, a sign of possible intra-abdominal sepsis. His temperature spiked further to 40°C, heart rate increased to 145 beats per minute, and his blood pressure continued to drop, recording at 80/50 mmHg. His respiratory rate also increased to 32 breaths per minute and his oxygen saturation further decreased to 84% despite maximum supplemental oxygen, indicating possible acute respiratory distress syndrome (ARDS).

New diagnostic results revealed an increased lactate level of 5.2 mmol/L, suggesting worsening tissue hypoperfusion. His creatinine level rose to 2.3 mg/dL and his BUN climbed to 35 mg/dL, indicating progressive acute kidney injury. A CT scan of the abdomen was ordered and showed free air under the diaphragm, suggesting a perforated viscus. An urgent surgical consult was sought. This critical turn necessitated immediate surgical intervention and even more aggressive medical management. The medical team was faced with the challenge of managing the patient's sepsis, acute kidney injury, possible ARDS, and now a surgical abdomen, all of which required astute clinical reasoning and prompt response.