Musculocutaneous latissimus dorsi flap Phalloplasty Surgery - Nursing Case Study
Pathophysiology
• Primary mechanism: The musculocutaneous latissimus dorsi flap phalloplasty involves harvesting a flap of skin, muscle, and blood vessels from the patient's back (the latissimus dorsi muscle), which is then sculpted into a phallus. The blood vessels are anastomosed to recipient vessels in the groin to ensure blood flow.
• Secondary mechanism: Nerve coaptation is performed by connecting the nerves in the flap to the recipient's ilioinguinal nerve to achieve tactile sensation. However, this does not provide erotic sensation, which is a limitation of this procedure.
• Key complication: Severe complications may include flap necrosis due to compromise in blood supply. This can lead to infection, tissue death, and need for debridement or additional surgery. Other complications may include donor site morbidity, such as seroma, wound dehiscence, and scarring.
Patient Profile
Demographics:
52-year-old, male, construction worker
History:
• Key past medical history: Uncontrolled diabetes type 2, hypertension, previous botched phalloplasty
• Current medications: Metformin, Lisinopril, Amlodipine
• Allergies: Penicillin, Iodine
Current Presentation:
• Chief complaint: Severe pain and infection at surgical site
• Key symptoms: Fever, chills, purulent discharge from surgical site, redness and swelling around the site, extreme tenderness, unable to urinate
• Vital signs: BP 180/105 mmHg, Heart rate 120 bpm, Respiratory rate 26/min, Temperature 39.2°C (102.5°F), Oxygen saturation 92% on room air.
Section 1
Change in patient status:
Despite administration of broad-spectrum antibiotics, the patient's condition continues to deteriorate. His vitals have shown little improvement with BP now at 185/110 mmHg, Heart rate 125 bpm, Respiratory rate 28/min, and a persistently high temperature of 39.5°C (103.1°F). His oxygen saturation has dropped to 88% on room air, indicating possible respiratory distress. His pain remains uncontrolled despite regular administration of analgesics and he has started to become increasingly restless and agitated, which might be a sign of delirium related to the infection and pain.
The surgical wound site has worsened, with increased redness, swelling, and a foul-smelling purulent discharge. Upon palpation, crepitus is felt under the skin, suggesting the presence of subcutaneous emphysema, a sign of gas-producing bacteria, possibly indicating necrotizing fasciitis. The patient also reports a deep, throbbing pain in the groin area and the inability to move his right leg without severe pain, suggesting a potential deep vein thrombosis. This could be a complication due to prolonged immobility and the patient's history of uncontrolled diabetes and hypertension. Furthermore, the patient's urine output has significantly decreased, raising concerns about possible acute kidney injury secondary to sepsis.
This constellation of symptoms suggests a rapidly deteriorating patient dealing with uncontrolled infection, pain, possible necrotizing fasciitis, deep vein thrombosis, and acute kidney injury. These complications require quick identification and management to prevent further deterioration and potential multi-organ failure.
Section 2
Change in patient status:
Despite vigorous attempts to stabilize the patient, his condition has further declined. His blood pressure has skyrocketed to 200/120 mmHg, heart rate has increased to 135 bpm, and respiratory rate is now at 32/min, indicating an escalating level of physiological stress. His temperature remains high at 39.8°C (103.6°F), and his oxygen saturation has further dropped to 84% on room air. The patient's consciousness level has also dropped, with him now being only rousable to pain, suggestive of a declining neurological status.
The surgical wound site has rapidly worsened, with the redness and swelling spreading to the surrounding skin. The wound now exhibits a black, necrotic appearance with increased purulent discharge and the crepitus has become more obvious, strongly suggesting a spreading necrotizing fasciitis. The patient's deep, throbbing pain in the groin area has intensified, and he now reports a heavy, aching feeling in the entire right leg, indicating a worsening deep vein thrombosis. His urine output has further decreased to less than 20 ml/hour, suggestive of an escalating acute kidney injury. His blood glucose levels are now at 350 mg/dl, despite insulin administration, indicative of stress hyperglycemia. This drastic decline points to a rapidly deteriorating patient with escalating uncontrolled infection, pain, necrotizing fasciitis, deep vein thrombosis, acute kidney injury and hyperglycemia, all requiring immediate and aggressive intervention to prevent imminent multi-organ failure.
Section 3
New Diagnostic Results:
Despite the aggressive interventions put in place, the patient's condition continues to deteriorate. His latest blood tests show markedly elevated inflammatory markers, with a C-reactive protein of 220 mg/L and a white blood cell count of 22,000 cells/µL, indicative of severe systemic infection. His coagulation profile is also abnormal, with a prolonged prothrombin time (PT) of 16 seconds and an elevated D-dimer of 3,000 ng/mL, suggestive of a disseminated intravascular coagulation.
The patient's serum creatinine has shot up to 3.5 mg/dL, confirming the suspicion of acute kidney injury. Lactate levels are also elevated at 5 mmol/L, pointing to tissue hypoxia and possible septic shock. The wound cultures have grown Streptococcus pyogenes, which is known to cause necrotizing fasciitis. A Doppler ultrasound of the right leg has confirmed extensive deep vein thrombosis.
These results correlate with the patient's worsening clinical picture and highlight the gravity of his situation. The escalating sepsis, uncontrolled infection, deep vein thrombosis, and acute kidney injury necessitate immediate, high-level interventions to prevent further deterioration and multi-organ failure. The team must utilize their critical thinking skills to manage these complex, interacting conditions and formulate an aggressive, multi-pronged treatment plan to give the patient the best chance of survival.
Section 4
Change in Patient Status:
Over the next 24 hours, the patient's condition takes a significant turn for the worse. He becomes increasingly lethargic and confused, indicative of a possible septic encephalopathy. His urine output drops to less than 20 mL/hr, a further sign of worsening renal function. He develops new-onset tachypnea with labored breathing and hypoxemia, with oxygen saturation levels dropping to 88% on room air. His blood pressure also starts to fluctuate, ranging from 90/60 to 160/100 mmHg, suggestive of autonomic dysregulation.
His physical examination reveals an erythematous, swollen, and extremely tender right leg, consistent with the diagnosed deep vein thrombosis and possibly worsening necrotizing fasciitis. The surgical site of the musculocutaneous latissimus dorsi flap phalloplasty is noted to be increasingly necrotic and foul-smelling. This rapidly declining clinical picture, combined with the laboratory findings, puts the patient at a high risk for imminent multi-organ failure. The team must act swiftly and decisively to manage the septic shock, uncontrolled infection, deep vein thrombosis, and acute kidney injury, all while monitoring for potential new complications.
Section 5
New Diagnostic Results:
Blood cultures are drawn and sent to the lab for analysis. The results confirm the suspected sepsis, revealing the presence of gram-negative bacilli, most likely Escherichia coli. The gram stain and culture results from the surgical wound also indicate the presence of mixed aerobic and anaerobic organisms, including Staphylococcus aureus and Bacteroides fragilis, indicative of necrotizing fasciitis. The patient's complete blood count (CBC) shows leukocytosis with a white blood cell count of 19,000/uL (normal: 4,500-11,000/uL) and a shift to the left with 85% neutrophils (normal: 40-70%). His serum lactate level is found to be 5 mmol/L (normal: 0.5-1 mmol/L), reflecting tissue hypoperfusion.
A Doppler ultrasound of the right leg confirms the extension of the deep vein thrombosis to the femoral vein. Moreover, a computed tomography (CT) scan of the abdomen shows dilation of the renal pelvis and hydronephrosis, suggesting post-renal acute kidney injury likely secondary to urinary tract obstruction or neurogenic bladder. The patient's serum creatinine has also sharply risen to 3.2 mg/dL (normal: 0.6-1.2 mg/dL) and blood urea nitrogen to 45 mg/dL (normal: 7-20 mg/dL), along with a decreased glomerular filtration rate of 30 mL/min (normal: >60 mL/min). These diagnostic findings necessitate immediate and aggressive intervention to prevent further deterioration of the patient's condition and potential multi-organ failure.