![]() īe aware pain can sometimes be difficult to assess or be absent if there is nerve damage, in polytrauma patients, a patient who is unconscious or sedated, and in children or patients who have had some form of regional nerve blocks for pain relief. In children, anxiety associated with increasing analgesic requirements is a reliable indicator of compartment syndrome. The absence of pulses is usually a late finding, and amputations are considered when there is a significant amount of ischaemic tissue death. ![]() Radial and ulnar pulses are usually intact, given the systolic arterial pressure (around 120 mmHg) usually exceeds the pressure within the involved compartment. Sensory deficits or paresthesias are usually signs of nerve ischemia in the affected compartment and can be present. A few patients who present a few hours after the onset of compartment syndrome present with hemorrhagic blisters in addition to the above mentioned. ![]() Pain can, however, disappear in late stages or presentations or chronic compartment syndrome. Pain is usually not relieved by rest, analgesia, or anti-inflammatory medication. Pain that is out of proportion to the injury is the pathognomonic sign, especially on passive stretching of the fingers. They present with a swollen, tense, tender forearm with overlying skin that is often pink. Patients often present within a few hours of the inciting event, sometimes even within 48 hours. Ĭompartment syndrome of the forearm is primarily a clinical diagnosis. The result is a dysfunctional muscle compartment with local and distant manifestations that depend on the compartment involved and the degree of muscle contracture and nerve damage. Associated nerve damage causes further muscle dysfunction, sensory deficits, and may result in chronic pain. When sustained vascular compromise occurs, the muscle undergoes necrosis, fibrosis, and contracture. They can survive up to 4 hours (neuropraxia), and at 8 hours, irreversible damage occurs. Nerves can conduct impulses for up to 1 hour. They can tolerate ischemia for up to 4 hours, and irreversible damage occurs at 8 hours. Vascularisation in the middle of the muscle belly is more affected, and that is when muscle degeneration occurs. Muscles centered around the anterior interosseous artery are the most commonly affected, particularly FPL and FDP. In the acute stage, nerves are involved because of ischemia, and in later stages, damage occurs due to entrapment of nerves in the fibrous tissue. Muscles can retain the electrical response for up to 3 hours. This leads to a shift in the interstitial and cellular osmolality, creating a vicious cycle of cellular anoxia, leading to chemical mediators further increasing capillary permeability. The increased pressure within the osseofascial compartment affects the venous return system, which results in decreased arterial pressure and an increase in venous pressure. Among them, the common factor tends to be anoxia at the cellular level following a cascade of events. There is more than one theory to describe the pathophysiology of compartment syndrome.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |