Pathophysiology, Diagnosis and Treatment, Fat Embolism - Coursework Example

Fat embolism Introduction With controversies about its causation, pathophysiology, diagnosis and treatment, fat embolism is a poorly understood subject (see Latif et al. 2008, pp. 408). This is so despite the fact that it has been medically known since it was first described in 1862 and clinically diagnosed in 1873. Description of FES Fat embolism occurs when fat globules enter the bloodstream and form emboli that alter the body’s organ systems. With fat globules lodged in the vasculature of human organs, one may develop quite a range of problems from renal failure and sudden loss of consciousness to a rapid spike in temperature due to cerebral emboli that besiege the hypothalamus. As such, fat embolism and its resultant fat embolism syndrome are serious and potentially life threatening condition (Hussain 2004). Very often, it occurs as consequence of blunt trauma – e.g., motor vehicles crashes or hip fractures for older adults -- that is complicated by long bone fractures, such as those involving the middle and proximal parts of the femoral shaft, bones of the pelvis and bones with marrow (Derstine & Hargrove 2001, pp. 448). Likewise, it is common after skeletal injury and is most likely to occur in patients who undergo orthopedic procedures – e.g., reaming for interemdullary nailing, and hip and knee replacements which involves injection of cement. However, fat embolism is observed to have similarly occurred too in association with acute pancreatic, diabetes mellitus, burns, joint reconstruction, liposuction, cardiopulmonary bypass, decompression sickness and pareteral influsion of lipids, sickle cell crisis and alcoholism (Latif et al., pp. 408; see also Gore & Lacey 2005; Derstine & Hargrove, pp. 448)). The effects of fat embolism syndrome may be mild and undetected in some cases, or severe and are can lead to multi-system dysfunction in other cases. It is the lungs that are always involved, followed by the brain (Latif et al., pp. 408; Gore & Lacey 2005). Its manifestations may be pulmonary, neurologic or dermatological. The earliest manifestations of fat embolism syndrome are pulmonary changes, including – among others -- tachypnoea, dyspnoes, cyanosis, hypoxaemia, chest pain, shortness of breath, rales and the “shock lung syndrome” (Latif et al., pp. 408; Simon, Sherman & Koenigsknecht 2007, pp. 82; Derstine & Hargrove, pp. 448). The neurologic signs range from acute confusion, headache, stupor, coma, rigidity or convulsions (Simon, Sherman & Koenigsknecht 2007, pp. 82; cf. Latif et al., pp. 408). And, dermatological changes are composed of appearance of reddish brown petechial rash within twenty-four to thirty-six hours to the upper body, chest, neck, upper arm, axilla, shoulders, oral mucus membranes and conjunctivae (see Latif et al., pp. 408). Other signs may also occur, but are non-specific – e.g., retinal changes, such as exudates, cotton wool spots, edema, hemorrhage, or intravascular fat globules, renal change presenting itself as lipuria, and hepatic change manifesting as jaundice (Latif et al., pp. 409). Besides these three signs and symptoms, it is manifested too by the changes in arterial blood gas levels and the fall in hermatocrit (Derstine & Hargrove, pp. 448). Pathophysiology/physiology There are currently two theories widely accepted by medical authorities explaining about the disturbance of body functions as caused by fat embolism syndrome. The first theory, also called the mechanical theory, maintains that fat globules cause mechanical occlusion of multiple blood vessels. This occlusion is oftentimes temporary or incomplete, because the fluid and deformable fat globules do not completely obstruct capillary blood flow (Latif et al., pp. 408). However, how the fat gets into the systemic circulation is still not clear. So far, what is known from exidence is that, as fractures – and repair of fractures -- increase the intramedullary pressure, the fat may enter the systemic circulation either through the venous drainage of the femur via a shunt between the arterial and venous systems in bone or through the pulmonary capillaries (Wilson, Grande & Hoyt 2007, pp. 473; see Nursing Care Plan for Fractures 2005)) from which the fat droplets travel through arteriovenous shunts to the brain (Kirkland 2009; see also Shaikh 2009). Now, microvascular lodging of fat droplets is responsible for local ischemia and inflammation, with concomitant release of inflammatory mediators, platelet aggregation and vasoactive amines (Kirkland 2009). Providing explanation on non-traumatic forms of fat embolism syndrome, the second theory – the biochemical theory – holds that hormonal changes caused by trauma and/or sepsis induce systemic release of free fatty acids as chylomicrons. These circulating free fatty acides are directly toxic to pneumocytes and capillary endothelium in the lungs; and they cause interstitial hemorrhage, edema and chemical pneumonitis. It is also possible that the coexisting shock, hypoyolemia and sepsis – all of which reduce liver flow – facilitate the development of fat embolism syndrome by exacerbating the toxic effects of free fatty acids (see Kirkland 2009; Latif et al, pp. 408; Shaikh 2009; see also Nursing Care Plan for Fractures 2005). Key nursing interventions Considering the nature of fat embolism and fat embolism syndrome, prevention and early detection understandably prove the cornerstone of treatment. And, in general terms, key nursing interventions for cases of fat embolism syndrome – which are characteristically supportive in nature – follow the approaches prescribed as pre-, intra- or post-operative stages (see Latif et al., pp.412). Pre-operative stage In case one suffers from usual antecedent of fat embolism syndrome, such as long bone fracture, a key treatment step is early stabilization of fractures (Simon, Sherman & Koenigsknecht, pp. 82). Immobilization of the patient – that is, permitting no excessive motion – has been shown to decrease the incidence of fat embolism syndrome. Nevertheless, there’s always a critical need to promptly recognize the symptoms of fat embolism syndrome especially in the first twenty-four to seventy-two hours after the patient is injured (Derstine & Hargrove, pp. 448). Diagnosis of FES relies primarily on clinical findings, with the so-called Gurd’s criteria serving as the framework. On account of nurse’s close contact with the patient, he/she is in the position to recognize signs or symptoms of fat embolism syndrome and intervene urgently (Gore & Lacey 2005). As in the case of all patients with other disease or conditions, a fundamental nursing intervention may take the form of assessment of the patients’ body systems and documentation of baseline data. In the concrete, the following interventions may be done: Monitoring of the patient’s vital signs every one to two hours and his/her Spo2 levels continuously, bearing in mind that a decrease in gas exchange may cause hypoxia with hyperventilation and tachycardia Continuously monitoring the patient’s heart for signs of fat embolism syndrome – such as sinus tachycardia, right bundle-branch block and ST-segment and T-wave abnormalities – for symptoms of decreased cardiac output such as hypotension, oliguria, pale or cool skin, decreased mental status, angina, arrhythmias, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, weakness and anorexia Keeping an eye on the results of patient’s complete blood cell count and sedimentation rate, chest X-ray, arterial blood gases (ABG), among others Strictly supervising the patient’s fluid intake and output for signs of decreased renal perfusion, or obtaining urine specimens for testing for the presence of fat globules Frequent assessment of patient’s neurovascular status, level of consciousness and skin In case of high suspicion of fat embolism syndrome, a fundoscopic examination can be done to assess the patient’s retina for blockages or petechiae The Gurd’s criteria helps to finalize the confirmation that a patient has fat embolism syndrome. The diagnosis is confirmed if the patient has one major and three minor criteria or two major and two minor criteria (Gore & Lacey 2005). The major criteria are: nonpalpable reddish brown petechial rash over the upper body in a vest distribution, particularly in the axillae (occurring within 24 to 36 hours of injury and resolving quickly); respiratory symptoms, bilateral chest X-ray changes, tachypnea, dyspnea, and hypoxia; and cerebral signs without cause: agitation, seizures, coma. To minor criteria belong the following: tachycardia; temperature greater than 101.30F or 38.50C; retinal hemorrhages with emboli present in the retina with opthalmoscopic examination; fat globules in urine or sputum; sudden decrease in hemoglobin and hematocrit levels and platelet count; and increase in sedimentation rate. Intra-operative stage When the patient is finally pronounced to have fat embolism syndrome, the nursing interventions that may be performed – after administering supplemental oxygen and contacting the orthopedic surgeon, are: Keeping the patient in a high Fowler’s position to promote easier breathing and administering oxygen or mechanical ventilation (for respiratory failure) as ordered Maintaining the stability of the patient’s fracture site until surgical stabilization is done Assessment of oxygenation with continuous Spo2 monitoring and ABG measurement as needed Keeping watch for dangerous clinical trends, such as with Pao2 level below 60 mm Hg patient would probably need intubation, mechanical ventilation, or even positive end-expiratory pressure to maintain arterial oxygenation Transfusing packed red blood cells (RBC) or platelets as ordered to re-establish normal circulating volume and reverse hypoxemia and hypotension Administering adequate fluids to flush fatty acids through the patient’s system so as to prevent kidney damage Monitoring the patient’s response to fluid resuscitation – if necessary, by pulmonary artery catheter Providing emotional support Post-operative stage Nursing interventions do not end the moment the patient is discharged from the hospital. This time, nursing intervention may take the form of providing education about the signs and symptoms of FES and disseminating information as regards how and when to notify primary care providers when signs and symptoms of fat embolism syndrome come to surface (again). Most importantly, education provided by nurses needs to focus on how to protect patients from fat embolism syndrome. The actions that may be prescribed are: Immobilization and stabilization of the patient’s fracture site, as avoiding excessive motions or movements may help prevent release fat globules into the patient’s circulation Have the patient cough and breathe deeply, or use incentive spirometry to prevent or minimize atelectasis and improve pulmonary function Maintenance of adequate oxygenation and support of patient’s respiratory status, especially if the patient develops abnormal breath sounds and respiratory distress, and administration of supplemental oxygen when needed Maintenance of the patient’s hydration with I.V. fluids as ordered to maintain urine output at more than 30 ml/hour and mean arterial pressure at greater than 60 mm Hg to prevent shock, perfuse the kidneys, and prevent mobilization of fat Administration of vasoactive medications as ordered to support the patient’s cardiovascular function Recording of baseline assessment findings and laboratory values, and frequent assessment of the patient for changes (see Gore & Lacey 2005). Conclusion Obviously, an understanding of fat embolism and fat embolism syndrome has seen improvement over the years – at least, since it was first detected in the 19th century. However, as indicated at the outset of this paper, there still are some areas that need to be researched on – i.e., its causation, pathophysiology, diagnosis, and even treatment. The privileged role and possible contribution of nurses in comprehending fat embolism and fat embolism syndrome more thoroughly are very obvious. For, as in most medical cases, the nursing professional finds himself/herself at the forefront of encountering the patients afflicted with fat embolism and fat embolism syndrome. References: Derstine, J.B. & Hargrove, S.D. (2001). Comprehensive rehabilitation nursing. Philadelphia: W.B. Saunders Company. Gore, T. & Lacey, S. (2005). Hospital nursing: bone up on fat embolism syndrome. Lippincot’s Nursingcenter.com, 35(8). Retrieved 2 September 2009, from http://www.nursingcenter.com/library/JournalArticle.asp?Article_ID=595360. Hussain, A. (2004). A fatal fat embolism. The Internet Journal of Anesthesiology 8(2). Retrieved 8 September 2009, from http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ija/vol8n2/fat.xml. Kirkland, L. (2009). Fat embolism. eMedicine. Retrieved 8 September 2009, from http://emedicine.medscape.com/article/460524-overview. Latif, A., Bashir, A., Aurangzeb & Ghani, U. (2008). Fat embolism and fat embolism syndrome. Professional Med J 15(4), pp. 407-413. Nursing care plan for fractures (2005). International Biopharm. Retrieved 2 September 2009, from http://nursingcareplanfractures.blogspot.com/. Shaikh, N. (2009). Emergency management of fat embolism syndrome. Journal of Emergencies, Trauma and Shock (serial online). Retrieved 8 September 2009, from http://www.onlinejets.org/text.asp?2009/2/1/29/44680. Simon, R.R., Sherman, S.C. & Koenigsknecht, S.J. (2007). Emergency orthopedics: the extremities. New York: McGraw Hill Companies, Inc. Wilson, W.C., Grande, C.M. & Hoyt, D.B. (2007). Trauma: critical care. New York: Informa Healthcare USA, Inc. Read More