The Clinical Manifestations of Compartment Syndrome
Discuss about the Pathophysiology Of Compartment Syndrome.
The case study shows that Leigh’s daughter does not understand about the pathophysiology of compartment syndrome. In order to understand the pathophysiology of compartment syndrome it is first important to understand the clinical manifestations and the definition of compartment syndrome. This report gives a vivid account of the pathophysiology of compartment symptoms along with the linkage of the symptoms with the case study
Acute compartment syndrome is caused when the circulation of the blood is hampered due to an increased pressure in a limited space and hence the function of the tissue is compromised, causing tissue ischemia, nerve damage and necrosis (Lawendy 2014).
In order to understand the pathophysiology of compartment syndrome it is important to understand the anatomy. Compartment are the groupings of the muscles and the tissues are covered with the help of a membrane called the fascia and all the compartments consists of a major nerve and also the blood vessels (Lawendy 2014). The compartment syndrome occurs when swelling occurs within these compartments, which can be referred to an augmentation of the interstitial pressure within a closed osseofacial compartment causing a microvascular conciliation (Mabvuure et al. 2012). It the condition persists or there is a delay in the diagnosis, then this can affect the future quality of the life. Some of the common site where the compartment syndrome occurs is the lower leg. The anterior compartment is the affected most frequently followed by the lateral compartment and the posterior compartment. An increase in the volume of the compartments can increase due to bleeding, intravenous fluid or due to ischemic swelling. Paik et al. (2013) have stated that compartment syndrome can also occur in the two compartment of the forearm. According to Willis (2012) unless the pressure is removed completely permanent necrosis of the tissues and disability can occur. The compartment syndrome can occur due to a fracture, a bruised muscle, a reestablished blood flow after a blocked circulation. It can also occur after an injured blood vessel is blocked for a long time. Lying in a position for a long time can also block the circulation of the blood within that particular area. Use of anabolic steroid can also result in compartment syndrome. Tight bandages and castes during a fracture can constrict blood flow and can initiate compartment syndrome. Fasciotomy remains the only effective treatment for decompressing the muscles. There is a wide cascade of the cellular and the molecular event that leads to compartment syndrome with an interplay between the interstitial surface and the capillary membrane in combination with the activation of the neutrophil and the hemodilution. The abdominal compartment syndrome is mainly caused due to the capillary leak resulting in the extravasation of the capillary fluid in to the massive bowel wall edema and interstitium.
As stated by Willis (2012), the compartmental size reduction can be brought about by several ways. The initial traumatic, surgical, hemorrhagic or vascular injuries stimulates the inflammatory reactions.
The Anatomy of Compartment Syndrome
The inflammatory response in the compartment syndrome is mainly caused due to the accumulation of the nutrients, clotting factors, macrophages, neutrophils to the site of damage.
As a result the damaged tissue initiates the chemotaxic mechanism by secreting the inflammatory mediators such as the prostaglandins, histamine and the cytokines. Hence the capillary permeability of the localized tissue increases. This leads to swelling, edema, pain and vasodilation resulting in pain and redness. It is to be noted that endothelium is not only an inert barrier between the blood vessels and the tissues but also acts as a metabolic organ that stimulates the anticoagulation pathways.
The increased capillary permeability during the inflammation causes swelling and increases the intra-compartmental pressure (ICP) (Gakuu 2014). Normally the compartments have fixed volumes and constriction of these compartments lessens the tissue perfusion. As a result the hydrostatic capillary pressure increases resulting in hypertension. Due to an increase in the hydrostatic pressure at the venous or the arterial end, edema occurs (Willis 2012). The blood pressure in the capillary rises resulting in the augmentation of the filtration rate. Due to this a larger amount of the fluid moves to the interstitial space causing the collection of more fluid within the compartments) (Gakuu 2014). An increased perfusion pressure is hence caused due to the rising ACP. With this rise of the ACP, the auto regulatory mechanism comes in to play causing the development of a cascade of injuries. Eventually the blood flow in to the tissue is reduced to that level when the tissue is no longer viable. The interstitial pressure exceeds the intravascular pressure causing the walls of the blood vessels to collapse and impending the further flow of the blood.
Local tissue ischemia and intracellular edema occurs that further reduces the ICP. Due to the inefficient supply of oxygenated blood anaerobic respiration occurs resulting in loss of adenosine triphosphate and disruption of the cellular membrane (Donaldson et al. 2014).
If the interventions are not started then the necrotic muscles would never recover and hence the seriousness of the condition should be never underestimated.
The intra-compartmental volume of the volume of the edema is thus increased. Due to the arterio-venous gradient theory the capillary blood flow may be compromised due to the increased venous pressure, reduced arterial pressure and an increased peripheral vascular resistance. After a period of ischemia the compartment symptoms sometimes occurs during the reperfusion (Willis 2012). At the time of the ischemia the intracellular reserves of the high energy phosphate bonds are depleted and it causes a buildup of the lactic acid along with an accompanying hydrogen ion and an increase in the intracellular reducing agent. Reperfusion may give rise to harmful effects other than preserving the normal muscle activity by removing the necessary precursors required for the adenine nucleotide synthesis (Von Keudell et al. 2015). The oxygen free radicals are produced by lipid peroxidation and calcium influx. According to Garner et al. (2014) white blood cells has been found to be important for the injury due to reperfusion. This damages the internal organs such as the heart, lungs, liver and the kidneys.
Causes of Compartment Syndrome
The two important signs and symptoms of compartment syndrome includes a persistent deep ache in an arm and a leg and parasthesia (tingling and abnormal sensation). The pain is mainly caused in the planter flexion of the foot. It is the cycle of events occurring in acute compartment syndrome that exceeds the venous pressure and disrupts the flow of the blood (Via et al. 2012). This lack of the oxygenated blood and the gathering of the waste products results in pain and decreased sensation in compartment syndrome. The excessive pressure buildup in the muscle compartments generates the pain (Willis 2012). The inflammatory response causes soup of the inflammatory mediators to activate the nociceptors evoking pain and sensitivity of the nocicptors, generating a hyperactive reaction to the stimuli.
Swelling of the muscle compartments is another feature of the compartment syndrome. As the fascia does not stretch, this can cause an increase in the capillaries, muscles and the nerves in the compartment. It has already been discussed that the ICP increases due to the capillary permeability which results in swelling (Von Keudell et al. 2015). Tingling or abnormal sensation is mainly caused by any kind of abnormalities in the peripheral nervous system. It is thought to be the abnormal showers of the impulses resulting from an ectopic focus and can arise from anywhere in the sensory pathway, from the sensory cortex to the peripheral nerves. Neuropathy is caused due to the compartment syndrome (Garner et al. 2014). A nerve at the injured site can get damaged or compressed resulting in acute pain. The entrapments of the lateral femoral nerve can also cause peripheral neuropathy due to compartment syndrome. The blood circulation from the high pressure arteries to the low pressure arteries is dependent on pressure differences between the blood vessels. As this difference decreases the rate of the oxygenated blood delivery and the drainage if the deoxygenated blood decreases. Due to this there is a collapse of the lymphatic vessels that causes ischemia resulting in paresthesia or tingling sensation in the early period (Garner et al. 2014).
Conclusion
Acute compartment syndrome can be considered as one of the true emergencies and can be considered as a devastating complication. It is associated with a vast range of inflammatory cascade that results in decreased blood flow in the muscles and finally muscle necrosis. If left untreated can lead to permanent disabilities. The treatments involves switching in to new methods of diagnosis and proper prophylactic and fasciotomy.
References
Donaldson, J., Haddad, B. and Khan, W.S., 2014. Suppl 1: the pathophysiology, diagnosis and current management of acute compartment syndrome. The open orthopaedics journal, 8, p.185.
Gakuu, L.N., 2014. Acute compartment syndrome. East African Orthopaedic Journal, 8(2), p.37.
Garner, M.R., Taylor, S.A., Gausden, E. and Lyden, J.P., 2014. Compartment syndrome: diagnosis, management, and unique concerns in the twenty-first century. HSS Journal®, 10(2), pp.143-152.
Lawendy, A.R., 2014. Pathophysiology of Compartment Syndrome.
Mabvuure, N.T., Malahias, M., Hindocha, S., Khan, W. and Juma, A., 2012. Suppl 3: Acute Compartment Syndrome of the Limbs: Current Concepts and Management. The open orthopaedics journal, 6, p.535.
Paik, R.S., Pepples, D. and Hutchinson, M.R., 2013. Chronic exertional compartment syndrome. BMJ: British Medical Journal (Online), 346.
Via, A.G., Oliva, F., Spoliti, M. and Maffulli, N., 2015. Acute compartment syndrome. Muscles, ligaments and tendons journal, 5(1), p.18.
Von Keudell, A.G., Weaver, M.J., Appleton, P.T., Bae, D.S., Dyer, G.S., Heng, M., Jupiter, J.B. and Vrahas, M.S., 2015. Diagnosis and treatment of acute extremity compartment syndrome. The Lancet, 386(10000), pp.1299-1310.
Willis, B., 2012. Compartment Syndrome. In Pediatric Orthopedic Surgical Emergencies (pp. 29-39). Springer, New York, NY.
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