Necrotizing Fasciitis: Pathophysiology, Role of Diabetes

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Table of Contents

Role of Diabetes in Necrotizing Fasciitis
Cause of Abdominal Pain
Pathophysiology of Fever
Analysis of Laboratory Results
Other Complications to Monitor
Standard Treatment
Rationale for using Hyperbaric Therapy
Wound Care Orders for Home Care
Discharge Instructions
References

Necrotizing Fasciitis is associated with different kinds of bacteria that cause damage to deeper skin and subcutaneous tissues (Cain, 2010). Actual destruction is done by toxic substances such as streptococcal pyogenic exotoxins produced by bacteria. These superantigen exotoxins can activate T-cells non-specifically, leading to excess production of cytokines. Excess cytokines cause excess immune response activities and inflammation, leading to severe systemic illnesses such as Necrotizing Fasciitis (Cain, 2010).

Role of Diabetes in Necrotizing Fasciitis

Necrotizing Fasciitis is common in people with a compromised immune system (Cain, 2010). Therefore, any infection that destabilization the immune system exposes a patient to Necrotizing Fasciitis. A poor immune system exposes one to bacterial infection. In the event of such an infection, the body becomes desperate to get rid of the intruders. This causes high defense activities at the point of infection, causing serious inflammation (Cain, 2010). According to Cain (2010), poor glycemic control in diabetic patients compromises the immune system by killing some defense cells such as neutrophils. In addition, tissue hypoxia that results from arteriosclerosis exposes diabetic patients to necrotizing fasciitis. Cain (2010) also observes that excess sugar provides food for bacteria making it difficult for wounds to heal.

Cause of Abdominal Pain

Fournier Gangrene is an infection that spreads so fast (Schroeder & Steinke 2005). Abdominal pain could mean that the infection has spread to the abdomen. In addition, testes originate from the abdomen right below the kidneys (Schroeder & Steinke 2005). Infection of the scrotum which extends to the testes can cause referred pain in the abdomen due to anatomical connections.

Pathophysiology of Fever

Body temperatures are controlled in the Hypothalamus (Schroeder & Steinke 2005). Exposure of vascular bed that surrounds hypothalamus to pyrogens initiates the production of prostaglandin E2 (Schroeder & Steinke 2005). When prostaglandin E2 crosses into the area of the hypothalamus that regulates temperatures, activities that lead to the rising of the setpoint are triggered. Raising the setpoint initiates chills and raised muscle tones in the body. The hypothalamus then responds by initiating activities such as vasoconstriction that lead to an increase in body temperature. Muscle shivers help in generating heat until temperatures match the new set point. For C.S, fever was caused by superantigens released by the bacteria. Although the use of fever in the infected body remains unclear, it is believed that the chemicals that trigger fever also stimulate production of body defence cells (Schroeder & Steinke 2005).

Analysis of Laboratory Results

Elevation of WBC signals infection. Reduction in Hemoglobin can impair oxygen transportation (McGee, 2005). Hematocrit which is a measure of red blood ratio in blood is low at 35% from the expected 37%-48% (McGee, 2005). This causes poor oxygen transportation. Elevation of neutrophils which fight bacteria indicates bacterial infection. Lymphocyte count of 3 is normal. Elevated glucose indicates that the patient is diabetic. Presence of diabetes and poor oxygen supply to tissues exposed this patient to NF (McGee, 2005).

A test score called Laboratory Risk Indicator for Necrotizing Fasciitis is used to determine presence of NF (McGee, 2005). For C-reactive proteins, score 4 is given if the count is equal to or more than 150mg/L and zero is given if the count is below 150. C.S having a count of 8 scores zero. For WBC, zero is given if the count is below 15cells/mm³, one is given if the count lies between 15 and 25 and 2 is given if the count is above 25. C.S scores 1. For hemoglobin, zero is given if the count is above 13.5g/dL, one is given if the count lies between 11 and 13.5 and 2 is given if the count is below 11. C.S having a count of 11.7 scores 1. Score 2 is given for a sodium count below 135mmol/L. C.S scores 2. Score 2 is given for a creatinine count below 1.6mg/dL. C.S scores 2. Score one is given if glucose count is more than 10mmol/L. C.S scores 1. The total score is 0+1+1+2+2+1=7. A total score above 6 indicates very high chances of NF (McGee, 2005). It should be noted that lab results cannot confirm NF. Confirmation can only be done by surgery through biopsy. However, due to NF’s ability to progress so fast, treatment should start immediately after seeing signs.

Other Complications to Monitor

Following the lab results, C.S is exposed to anaemia due to a reduction in Hematocrit. The blood sugar should also be monitored for diabetes (McGee, 2005). Kidney impairment should also be investigated considering the increase in creatinine level.

Standard Treatment

Treatment for necrotizing fasciitis is surgical debridement (Jain et al. 2009). This is a process through which damaged tissues are removed to prevent spreading and speed up healing process. Debridement is combined with antibiotics such as piperacillin and vancomycin which control bacterial activities by interfering with their cell wall formation (Jain et al. 2009). Jain et al. (2009) noted that culture should be done to determine appropriate drugs. Because necrotizing fasciitis is associated with hypoxia, oxygenation of affected tissues is done to stop spreading of the infection (Jain et al. 2009).

Rationale for using Hyperbaric Therapy

In hyperbaric therapy, pure oxygen is availed as treatment (Salcido, 2007). According to Salcido (2007), atmospheric pressure is raised in a well-controlled room containing pure oxygen. This allows the patient to inhale 100% oxygen. Hyperbaric therapy is administered in conditions characterised by shortage of oxygen in tissues such decompression sickness (Salcido, 2007). The therapy is also used to treat wounds that resist healing in diabetic patients. In this case, availing high pressured pure oxygen ensures that the lungs take up more than three times the normal oxygen intake. The oxygen is then distributed throughout the body. Presence of high oxygen stimulates production of growth factors and stem cells which facilitate healing (Salcido, 2007).

Wound Care Orders for Home Care

Since it is difficult for wounds to heal in diabetic patients, C. S. should not fail to take insulin to control blood sugar (Magel, 2008). The patient should also take a right diet including enough proteins and calories which promote healing. Fluids should be taken for hydration. The patient should also observe cleanliness and stay in a room with sufficient air supply for maximum oxygenation (Magel, 2008). Wound dressing should be done properly without imposing too much pressure to allow cell proliferation and faster healing.

Discharge Instructions

NF patients need a lot of monitoring. However, once the situation is under control, patients should be given instructions that would maximise healing outcomes and prevent readmission. Instructions regarding sugar level management should be given (Magel, 2008). Patients should be instructed to ensure their glycated haemoglobin level does not go beyond seven percent. All needles have to remain capped unless they have to be used immediately and should not be recycled (Magel, 2008). Magel (2008) asserts that before any injection is done to either administer insulin or test blood sugar, the point of injection must be thoroughly cleaned. After injection, the area should again be wiped with alcohol pad to avoid infection. The patient should be given instructions with regard to home care wound management. Since NF can completely change the patient’s life, Magel (2008) says that nurses should help in arranging for social services that would improve coping. Physical therapies should also be advised to help the patient regain maximum physical functioning (Magel, 2008).

References

Cain, S. (2010). Necrotizing fasciitis: recognition and care. Practice Nursing Journal. 21(6):297-302.

Jain, A., Varma A., Mangalanandan K. & Bal A. (2009). Surgical outcome of necrotizing fasciitis in diabetic lower limbs. Journal of Diabetic Foot Complications, 1 (4): 80–84

McGee, E.J. (2005). Necrotizing Fasciitis: Review of pathophysiology, diagnosis, and treatment. Critical Care Nursing Quarterly, 28(1), 80-84.

Magel, D. C. (2008). The nurse’s role in managing necrotizing fasciitis. AORN Journal. 88(6):977-982.

Salcido, R. (2007). Necrotizing Fasciitis: Reviewing the causes and treatment strategies. Journal of Advances in Skin & Wound Care, 20: 288-293.

Schroeder, J.L & Steinke, E.E. (2005). Necrotizing Fasciitis: The importance of early diagnosis and debridement. Association of Operating Room Nurses Journal, 82(6), 1031-1040

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