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1 Program Information

2 Muscular System Suresh Agarwal, M.D.
This presentation will review topics relating to the muscular system that are pertinent to critical care.

3 Muscular System Neuromuscular Physiology Neuromuscular Disorders
Compartment Syndrome Rhabdomyolysis The goals of this presentation are to review neuromuscular physiology, discuss some common neuromuscular disorders, discuss compartment syndrome, review information regarding rhabdomyolysis.

4 Neuromuscular Physiology: The Motor Unit
Lower Motor Neurons = Alpha Motor Neurons Alpha Motor Neuron Cell Bodies Cranial Musculature: In the Brainstem Somatic Cells: In the Anterior Horn of the Spinal Cord Nerve Roots Plexus Peripheral Nerves Terminal Ramifications Motor Neuron Synapse Lower motor neurons that conduct motor function signals are called “alpha motor neurons.” The cell bodies of alpha motor neurons are in 2 locations based on their target muscles. Alpha motor neurons that conduct signals to the cranial musculature have cell bodies that reside in the brainstem. Alpha motor neurons that conduct signals to the somatic cells are in the anterior horn of the spinal cord. Motor axons emerge through the dura, traveling from the brainstem or spinal cord, as nerve roots. The motor axons coalesce with other motor axons, sensory fibers, and autonomic fibers to form a plexus. The plexi then travel in peripheral nerves, coursing toward the muscles that they innervate. The alpha motor neurons are myelinated, resulting in increased speed of signal conduction. When the alpha motor neuron arrives at its target muscle, multiple terminal ramifications, or tiny branches, form many connections with the muscle, resulting in synapses on individual muscle fibers. palrehab.net/images/spin20.jpg

5 The Motor Unit Neuromuscular Junction
Presynaptic Acetylcholine Release Postsynaptic Acetylcholine Binding Increases Muscle End-Plate Potential Threshold Level > Depolarizes Calcium Ions Released from Sarcoplasmic Reticulum Excitation-Contraction Coupling > Muscle Contraction Acetylcholine Degraded by Cholinesterase education.vetmed.vt.edu/Curriculum/VM8054/Labs/Lab10/IMAGES/MOTOR%20END%20PLATES%20SMALL%201.jpg The alpha motor neuron communicates, or synapses, with muscle fiber at the neuromuscular junction. On the presynaptic side of the neuromuscular junction, acetylcholine is constructed, parceled, and stored for release. A signal then comes down from the brain, traveling through the alpha motor neuron in the anterior horn of the spinal cord, then through the axon to the target muscle. This signal causes depolarization of the presynaptic membrane, activating voltage-gated calcium channels. The acetylcholine packets are then draw to the presynaptic membrane, fuse with it, and then are expelled from it into the synaptic cleft. The acetylcholine migrates to the postsynaptic membrane, where they bind to receptors that cause an influx of sodium, resulting in an increased muscle endplate potential, and eventually causing muscle depolarization. Depolarization causes calcium ions to be released from the sarcoplasmic reticulum. Muscle contraction is a result of excitation-contraction coupling. The acetylcholine then gets degraded by cholinesterase. Choline is returned to the presynaptic membrane, where it is recycled. bp3.blogger.com/_v2GFIISzHOU/SAjilu3b8kI/AAAAAAAAASk/3BRF9vWKgYY/s400/Neuro-Muscular+Junction.jpg

6 Neuromuscular Disorders
Neuromuscular diseases leading to critical illness Guillain-Barre Syndrome West Nile Virus Acute Flaccid Paralysis Syndrome Myasthenia Gravis Neuromuscular diseases caused by critical illness Critical Illness Polyneuropathy & Myopathy There are several neuromuscular diseases that might lead to critical illness. Conversely, there are neuromuscular diseases that might result from critical illness.

7 Neuromuscular Disorders
Acute Inflammatory Demyelinating Polyradiculoneuropathy (a.k.a. Guillain-Barre Syndrome) Motor >>Sensory Peripheral Neuropathy Monophasic Nadir at 4 weeks Immune mediated Exact etiology unknown Demyelinating Neuropathy Primary Axonopathy Acute Inflammatory Demyelinating Polyradiculoneuropathy is otherwise known as Guillain-Barre Syndrome. It is a peripheral neuropathy that affects motor nerves much more than sensory nerves. It has a monophasic course with nadir at approximately 4 weeks. The disease process appears to be immune mediated, with antibodies directed against components of the peripheral nerves. The exact etiology is still not clearly understood. Most patients undergo a demyelinating neuropathy. Approximately 5% suffer from a primary axonopathy.

8 Guillain-Barre Syndrome
? Preceding disease or condition Gangliosides Campylobacter jejuni Many different diseases and conditions have been implicated as the trigger for Guillain-Barre Syndrome. However, no single factor has been common to all cases of Guillain-Barre. There is however, a clear-cut link between the inflammatory response and the onset of Guillain-Barre. It is possible that antibodies are activated in response to the infection or condition and then the antibodies crossreact with peripheral nerve gangliosides. For example, antibodies against specific gangliosides have been identified following infection with Campylobacter jejuni. upload.wikimedia.org/wikipedia/commons/thumb/b/ba/Campylobacter.jpg/450px-Campylobacter.jpg

9 Guillain-Barre Syndrome
Clinical Findings Subacute Progressive weakness Starts in legs Sensory complaints No objective sensory deficits Diminished or absent deep tendon reflexes Myelin Clinical findings associated with Guillain-Barre Syndrome include a subacute onset of symptoms. The weakness begins in the legs and is progressive. Sensory complaints are often present with no findings consistent with sensory deficits. Deep tendon reflexes may slowly vanish after several days, so the patient may present with absent or diminished reflexes. upload.wikimedia.org/wikipedia/commons/c/c1/Myelinated_neuron.jpg drdavis.typepad.com/.a/6a00d834525ed169e201156f86664c970c-320pi

10 Guillain-Barre Syndrome
CSF findings, around 2nd week Elevated protein No pleocytosis The diagnosis of Guillain-Barre is based primarily on disease course and clinical findings. CSF examination can be used to exclude other potential diagnoses. CSF findings usually start to appear around the second week and consist of elevated protein content without pleocytosis. neuromuscular.wustl.edu/pics/diagrams/emg/gbsrecov.gif

11 Guillain-Barre Syndrome
Electrodiagnostic Studies Motor and Sensory Nerve Conduction Studies Needle Electromyography Findings: Segmental nerve demyelination Multifocal conduction blocks Slow Conduction Velocity Consistent with a Peripheral Neuropathy Electrodiagnostic studies, consisting of motor and sensory nerve conduction studies and Needle electromyography, can be used to substantiate the diagnosis of Guillain-Barre. The findings are consistent with segmental nerve demyelination, multifocal conduction block, and slow conduction velocities. These findings are consistent with a peripheral neuropathy. graphics8.nytimes.com/images/2007/08/01/health/adam/9238.jpg

12 Guillain-Barre Syndrome
Management Vent support Autonomic Dysfunction Immunotherapy Plasma exchange High dose IVIg Rehabilitation Management of Guillain-Barre Syndrome is primarily supportive. -The patient should be monitored and if they progress to respiratory failure, should be intubated early. Full ventilatory support is often necessary for a week or more. Most patients are able to be extubated within 4 weeks. -Autonomic dysfunction often presents as a hypersympathetic state with unexplained sinus tachycardia. The patient may have hyperdynamic vital signs with bradycardia in response to vagal stimulation or viscus distention. Temporary pacing may be necessary. This is one of the major causes of death attributable to Guillain-Barre Syndrome -Immunotherapy is aimed at eliminating the antibodies directed against the peripheral nerves. Plasma exchange or high dose IVIG is often used to accomplish this. Both appear to be equivalent. Corticosteroids have not demonstrated a benefit in the treatment of Guillain-Barre Syndrome. repairstemcell.files.wordpress.com/2009/03/ms-pic.jpg

13 West Nile Virus West Nile Virus Acute Flaccid Paralysis Syndrome
Flavivirus Birds and mosquitoes (Culex) Late summer or Fall West Nile Virus surfaced as a formidable neuromuscular disorder in 1999, during the outbreak in New York City. West Nile virus is a type of flavivirus. It is transmitted between birds and mosquitoes primarily. The Culex mosquito is responsible for the spread to humans. Clinical disease usually appears around late summer or fall. It is capable of being transmitted through blood. media.publicbroadcasting.net/kera/newsroom/images/ jpg

14 West Nile Virus 3 Different Clinical Manifestations
Asymptomatic infection Mild febrile syndrome West Nile Fever approx. 20% 3 – 6 days duration Neuroinvasive disease West Nile meningitis or encephalitis approx. 1 in 150 West Nile Virus has 3 distinct clinical manifestations: First, infection may be asymptomatic. Second, the infecton may be associated with a mild febrile syndrome, termed West Nile Fever. The is the case for approximately 20% of infected people. The syndrome typically lasts for 3 to 6 days. Third, approximately 1 in 150 with have neuroinvasive disease, termed West Nile meningitis or encephalitis t2.gstatic.com/images?q=tbn:vSeOC3WZ2Wee0M:http://news.bbc.co.uk/nol/shared/spl/hi/health/03/travel_health/diseases/img/westnile.jpg

15 West Nile Virus Acute Flaccid Paralysis Syndrome “poliomyelitis-like”
Ventral Horns and Ventral Roots Acute Asymmetrical Flaccid No Sensory Deficits No diffuse reflex deficits No bowel or bladder dysfunction Acute Flaccid Paralysis Syndrome is a constellation of symptoms resulting in loss of neuromuscular function. The paralysis is similar to that which is seen with polio. The lesions are localized to the ventral horns or ventral roots. The paralysis is acute in onset and results in asymmetrical flaccid paralysis. Notably there is no evidence of sensory deficits, diffuse reflex deficits, or bowel or bladder dysfunction.

16 West Nile Virus – Acute Flaccid Paralysis Syndrome
Electrodiagnostic testing Normal sensory potentials No findings of segmental demyelination (unlike Guillain-Barre) Low amplitude muscle action potentials I n affected areas Significant denervation changes in affected areas MRI CSF Mild pleocytosis (lymphocytic) Mild to Moderate increase in protein No change in glucose Electrodiagnostic findings associated with acute flaccid paralysis syndrome Diagnosis of this syndrome can be diagnosed

17 West Nile Virus – Acute Flaccid Paralysis Syndrome
Diagnosis Reverse-transcriptase PCR (insensitive) Antibody-capture ELISA (IgM) Treatment Supportive ?IVIg ?Antiretroviral medications Prognosis for recovery of strength is poor When suspected, West Nile Virus associated Acute Flaccid Paralysis Syndrome can be confirmed by the findings of West Nile virus RNA in the patients serum, CSF, or other tissues, identified with reverse-transcriptase polymerase chain reaction. This test is however insensitive. An alternate and more sensitive test is the identification of West Nile virus IgM in the patient’s CSF or serum with the antibody-capture enzyme-linked immunosorbent assay. The treatment for acute flaccid paralysis is still largely supportive. Treatment with IV immunoglobulin and antiretroviral medications has been attempted without significant success. The prognosis for recovering strength is poor.

18 Myasthenia Gravis Autoimmune attack on acetylcholine receptor
Fluctuating weakness Progressive with sustained exertion Incidence: Early adulthood: Women > Men Later adulthood: Women = Men Myasthenia gravis is another neuromuscular disease, caused by an autoimmune attack on the acetylcholine receptor of the postsynaptic membrane. Acetylcholine binding is blocked by the antibody. When the number of available receptors reaches 30%, the patient becomes symptomatic. This leads to fluctuating weakness that is worse after sustained exertion. Cardiac and smooth muscle are not affected. While the incidence is greater in young women than young men, the incidence becomes equal later in life

19 Myasthenia Gravis Clinical Presentation Muscle fatigue
Worst with prolonged exertion Ocular muscles Ptosis Diplopia Bulbar muscles Dysphagia Dysarthria Respiratory Failure Ocular muscles are frequently involved with myasthenia gravis leading to ptosis, as is seen here, and diplopia. The bulbar muscles are also often disturbed, leading to dysphagia and dysarthria. Along with these cranial nerve findings, respiratory failure is a common presenting symptom of myasthenia gravis.

20 Myasthenia Gravis Diagnosis Clinical presentation Edrophonium testing
Electrophysiologic studies Repetitive nerve stimulation Antibody Testing Acetylcholine receptor Muscle specific receptor tyrosine kinase (MuSK) The diagnosis of myasthenia gravis is frequently suspected based on clinical presentation. It can be confirmed with several tests, including edrophonium testing, electrophysiologic studies with repetitive nerve stimulation, and antibody testing, specifically for acetylcholine receptor antibodies and muscle specific receptor tyrosine kinase (MuSK) antibodies.

21 Myasthenia Gravis Myasthenic Crisis 20% of patients with MG
Respiratory failure Precipitating factors Bronchopulmonary processes Aspiration Sepsis Surgical procedures Immune modulation tapering Corticosteroids Pregnancy Certain Drugs Neuromuscular blocking agents Sensitive to Nondepolarizing agents Resistant to Depolarizing agents Thymomas More fulminate disease 30% of patients with myasthenic crisis Myasthenic crisis occurs in approximately 20% of patients with myasthenia gravis. These patients present with respiratory failure, requiring mechanical ventilation. There are many common precipitating factors including bronchopulmonary processes, aspiration, sepsis, surgical procedures, rapid immune modulation tapering, initiation of therapy with corticosteroids, preganancy, and certain drugs. Patients with myasthenia gravis are extremely sensitive to nondepolarizing neuromuscular blocking agents. They are resistant to Depolarizing neuromuscular blocking agents. Thymomas are a common finding in patients with myasthenia gravis. They are associated with a more fulminate disease course and are found in about 30% of patients with myasthenic crisis.

22 Myasthenia Gravis Treatment Immunomodulating Methods
Plasma exchange (short-term) Myasthenic crisis Surgical preparation Increased strength after 2 to 3 exchanges IVIg (short-term) Alternative to plasma exchange Possible longer period until onset of effect Corticosteroids Occasionally used Prolonged crises Transient increase in weakness One of the components of treatment for myasthenia gravis is aimed at immunomodulation. Plasma exchange is an effective short-term treatment in most patients. It is employed for the treatment of myasthenic crisis and surgical preparation for MG patients. Strength begins to show a rise after approximately 2 to 3 exchanges. In patients who have a contraindication to plasma exchange such as poor vascular access or sepsis, IVIg can serve as an alternative. It’s an effective short-term treatment as well. The period of time until the onset of effect can be significantly longer. Corticosteroids are occasionally used for treatment of prolonged crises and crises refractory to the above treatments. If started early in the disease course, steroids can lead to a transient increase in weakness and may prolong the time that mechanical ventilation is required. This phenomenon has not been observed when steroids are started later in the hospitalization.

23 Myasthenia Gravis Treatment Cholinesterase inhibitors
Cholinergic Crisis Possible increase in weakness Muscle fasciculations Muscarinic symptoms Avoid repeated/escalating doses Discontinue after intubation Acetylcholine Receptor Cholinesterase inhibitors are often used to attempt to ward off an impending myasthenic crisis. However, overzealous use can precipitate a cholinergic crisis. Signs of a cholinergic crisis include increased weakness, muscle fasciculations and symptoms associated with muscarinic symptoms such as miosis, lacrimation, salivation, abdominal cramping, nausea, vomiting, diarrhea, diaphoresis, and bradycardia. upload.wikimedia.org/wikipedia/commons/6/6e/Nicotinic_Acetylcholine_receptor.png

24 Myasthenia Gravis Thymus Abnormal in 75% Thymoma in 25% Thymectomy
Benign Malignant Thymectomy Necessary for thymoma Controversial for patients without know thymic abnormalities Disease course often abates Myasthenia gravis has a strong association with irregularities of the thymus. Up to 75% of patients have abnormal thymuses. Approximately 25% have thymomas, which may be benign or malignant. Thymectomy is therefore necessary in cases of thymoma. In patients who do not have known thymic abnormalities, the role for thymectomy is controversial. Following thymectomy, many patients experience cessation of symptoms.

25 Critical Illness Polyneuropathy & Myopathy
Generalized weakness Axonal Predisposing Factors Critical Illness Sepsis Multiple system organ failure Prolonged mechanical ventilation Critical illness polyneuropathy and myopathy is the chief cause of new-onset generalized weakness in ICU patients who are not being treated for a primary neuromuscular disorder. This condition is primarily due to axonal pathology, as opposed to the demyelinating neuromuscular disorders such as Guillain-Barre Syndrome. Predisposing factors include critical illness, sepsis, and multiple system organ failure. It results in a need for mechanical ventilation for a prolonged period.

26 Critical Illness Polyneuropathy & Myopathy
Common Antecedents Sepsis Multiple System Organ Failure Pathophysiology ICU days Number of invasive procedures Hyperglycemia Hypoalbuminemia Severity of MSOF Neuromuscular Blocking Agents Corticosteroids The factors that lead to critical illness are not fully understood. Sepsis and multiple system organ failure are common to all patients who develop this disorder. Factors that correlate with disease are days spent in critical care, number of invasive procedures, hyperglycemia, hypoalbuminemia, severity of multiple system organ failure, neuromuscular blocking agents, and corticosteroids.

27 Critical Illness Polyneuropathy & Myopathy
Clinical Features Muscle weakness and wasting Parasthesias Distal Sensory Loss Deep Tendon Reflexes Diminished or absent Clinical features include extremity muscle weakness and wasting, parasthesias, and distal sensory loss. Deep tendon reflexes may be diminished or absent. Few cases have been associated with facial or oropharyngeal weakness, differentiating from Guillain-Barre syndrome in which they are common. vasculitis.med.jhu.edu/typesof/images/Muscle_waste_MPA.jpg

28 Critical Illness Polyneuropathy & Myopathy
Nerve Conduction Normal nerve conduction speed Decreased muscle action potential amplitude Decreased sensory nerve action potential amplitude Needle Electrode Denervation Histopathology Primary axonal degeneration Electrodiagnostic studies are important in establishing the diagnosis of critical illness polyneuropathy and myopathy. Nerve conduction studies typically demonstrate normal conduction velocities with greatly decreased muscle action potential amplitudes and decreased sensory nerve action potential amplitudes. Needle electrode studies demonstrate changes consistent with denervation, greatest in the distal extremities. Histopathologic studies of peripheral nerves demonstrate diffuse primary axonal degeneration among both motor and sensory nerves.

29 Critical Illness Polyneuropathy & Myopathy
Prognosis Underlying critical illness Increased ventilator dependence Functional recovery in several months Padding and Positioning to prevent compression neuropathies Ulnar Nerve Compression The prognosis for patients suffering from critical illness polyneuropathy and myopathy is dependent on recovery from the underlying critical illness. This disorder results increased ventilator dependence with difficulty weaning. Nevertheless, most patients achieve full functional recovery within several months. During critical care and while the patient recovers from the generalized weakness and sensory deficits, stringent attention should be paid to padding and positioning to prevent compression neuropathies, which carry a worse prognosis. meddb.eznetpublish.ihealthspot.com/portals/2/MedicalLibraryAssets/Medical/CubitalTunnel_small.jpg

30 Compartment Syndrome Open or Closed Fractures Fixed Compartment
Tissue edema and bleeding Blood flow impeded Capillaries Arterioles Factors effecting tissue necrosis Amount of Pressure Duration of increased pressure Sensitivity of the tissue to ischemia One of the most common disorders of the muscular system frequently seen in the critical care is compartment syndrome. Compartment syndrome is often the result of trauma. It can occur with both open and closed fractures due to increased pressure within a fixed compartment. Following trauma, tissue edema and bleeding occur around the site of injury. If the pressure is too high, the capillaries and arterioles become compressed, unable to expand and deliver blood to the surrounding tissues. With compartment syndrome, the amount of tissue necrosis is dependent on several factors, including the amount of pressure in the compartment, the duration of the elevated pressure, and the sensitivity of that tissue to ischemia. Right Buttock Compartment Syndrome casesjournal.com/content/figures/ gif

31 Compartment Syndrome Tissue Ischemia Nervous tissue Muscle
Functional abnormalities after 30 minutes Irreversible damage after 12 to 24 hours Muscle Functional abnormalities after 2 to 4 hours Irreversible damage after 4 to 12 hours Increased capillary permeability -> Edema Necrotic Muscle Tissues have different sensitivities and tolerance for ischemia. Nervous tissue is relatively tolerant with functional abnormalities developing after 30 minutes of ischemia but not progressing to irreversible damage until after 12 to 24. In contrast, muscle does not start to develop functional abnormalities until 2 to 4 hours after the onset of ischemia. However irreversible necrosis develops after only 4 to 12 hours of ischemia. As the compartment syndrome continues to progress and capillaries become more permeable, edema within the compartment continues to increase, accelerating the rate of tissue necrosis.

32 Compartment Syndrome Risk factors Severity of fracture
Extent of soft tissue injury Compressive devices Anti-shock trousers Tourniquets Systemic hypotension Risk factors that amplify the rate of tissue death include severity of the fracture and extent of soft tissue injury. The use of compressive devices to control hemorrhage, such as anti-shock trousers and tourniquets, cause tissue ischemia and subsequent reperfusion injury with a corresponding rise in tissue edema. The patient is therefore more likely have a compartment syndrome if these devices are used and correlating with their duration of use. The presence of systemic hypotension decreases muscle perfusion, as would be expected and subsequent compartment syndrome with tissue ischemia is more likely.

33 Compartment Syndrome Most common location = Anterior Compartment of the Lower Leg Usually from closed tibia fracture Other sites Thigh Arm Buttock Foot The most common cause of acute compartment syndrome is traumatic injury with fractured bones. The most common site of acute compartment syndrome is the anterior compartment of the lower leg after closed tibia fractures. Other common sites of compartment syndrome are the thigh, arm, buttock, and foot. orthoinfo.aaos.org/figures/A00204F01.

34 Compartment Syndrome Diagnosis Clinical Tense compartment to palpation
Severe pain with passive range of motion Severe compartment tenderness Impaired sensory exam Decreased distal perfusion Pulseless = Too Late Extensive tissue necrosis present Serial Exams are Critical The diagnosis of compartment syndrome is clinical, based primarily on mechanism of injury, events following injury, symptoms and physical exam. On physical exam, the compartment is tense to palpation. The patient will have exquisite pain with passive range of motion and severe tenderness to palpation. The patient may have parasthesia and decreased sensation as the compartment syndrome progresses. As it becomes advanced, perfusion to the distal limb becomes compromised and may be mottled and cool with poor capillary refill. The limb will become pulseless if no intervention is taken. At this point, there is little chance of limb salvage as extensive tissue necrosis is present. Serial exams are critical in preventing the patient from reaching this stage by intervening before significant damage is done.

35 Compartment Syndrome Measurement of Compartment Pressures
Unresponsive patients Pressure > 30 to 45 = Indication for Fasciotomies Diastolic BP – Compartment Pressure < 30 = indication for Fasciotomies Compartment pressures can be monitored in unresponsive patients who are unable to relay sensation using. If the compartment pressure is greater than 30, surgical treatment is warranted. Also, if the diastolic blood pressure minus the compartment pressure is less than 30, fasciotomies are warranted. 35

36 Compartment Syndrome Treatment Surgical Fasciotomies
Fasciotomy within 12 hours = 68% normal functional result Hydration Monitor electrolytes Monitor for infection of fasciotomy sites If compartment syndrome is diagnosed, the patient should undergo fasciotomies emergently to restore perfusion to the limb. Fasciotomies must be sufficient to allow for adequate decompression. If performed within 12 hours, there is a 68% chance that the patient will have a normal functional outcome. Hydration is important in order to prevent renal failure as a result of rhabdomyolysis. Also, due to the risk of rhabdomyolysis and renal failure, electrolytes should be monitored closely. The fasciotomy sites must be monitored for infection. upload.wikimedia.org/wikipedia/commons/d/da/Fasciotomy_leg.jpg

37 Lower Leg Fasciotomies
2 incisions 4 compartments Anterolateral Incision Anterolateral Incision The most common site of compartment syndrome is the lower leg. The most reliable procedure for decompression is two-incision, four-compartment fasciotomies. The lateral incision is performed 1 to 2 cm anterior to the edge of the fibula. Extend the incision down through the skin and subcutaneous tissue. Use caution to avoid the minor saphenous vein and the peroneal nerve. Divide down to the fascia. Deep to this incision is the intermuscular septum that divides anterior and lateral compartments. The septum should be incised along the full length of the compartments in an “H” shape with transverse incisions at the two ends and a longitudinal incision between. The deep peroneal nerve should be located to ensure entry into both compartments. Anterolateral Incision img.medscape.com/pi/emed/ckb/orthopedic_surgery/ jpg

38 Lower Leg Fasciotomies
Medial Incision Incision 1 fingerbreadth posterior to medial edge of the tibia Liberal Length Avoid saphenous vein Divide fibers of soleus from tibia Neurovascular bundle Posteriomedial Incision Posteriomedial Incision For the medial incision, incise approx 1 fingerbreadth posterior to the medial edge of the tibia. A liberal incision should be made and carried down through the skin and subcutaneous tissue to the level of the fascia with careful attention to avoid the saphenous vein. In order to enter the deep posterior compartment, sharply and bluntly separate the muscle fibers of the soleus from the tibial edge. Identification of the neurovascular bundle ensures that the deep posterior compartment has been entered. img.medscape.com/pi/emed/ckb/orthopedic_surgery/ jpg

39 Upper Leg Fasciotomies
3 Compartments Anterior Posterior Medial Compartment syndrome rare 3 compartments blend with the hip Lateral incision usually sufficient Occasionally requires medial incision The upper leg has 3 compartments: anterior, posterior, and medial. Compartment syndrome is rare because of the large volume required to increase interstitial pressure. Also, the 3 compartments blend with the hip, so blood is able to exit from the compartments. If a compartment syndrome is identified, a lateral incision is usually sufficient. Occasionally a medial incision may be necessary.

40 Foot Compartment Syndrome
Interosseus or Intrinsic Compartment 4 intrinsic muscles between 1st and 4th metatarsals Medial Compartment Abductor hallicus and flexor hallicus brevis Central or Calcaneal Compartment Flexor digitorum brevis, quadratus plantae, and the adductor hallicus Lateral Compartment Flexor digiti minimi brevis, abductor digiti minimi There are 4 compartments in the foot: the Interosseus or Intrinsic Compartment, which contains the 4 intrinsic muscles between 1st and 4th metatarsals, the Medial Compartment, containing the abductor hallicus and flexor hallicus brevis, the Central or Calcaneal Compartmentm with the flexor digitorum brevis, quadratus plantae, and the adductor hallicus, and the Lateral Compartment, which contains the flexor digiti minimi brevis, abductor digiti minimi. All 4 compartments must be released.

41 Foot Compartment Syndrome
- Up to 10% of calcaneal fractures 41% of crush injuries to the foot No classic sign of CS Most reliable sign: tense bulging tissue Up to 10% of patients presenting with calcaneal fractures may have a compartment syndrome. Up to 41% of crush injuries to the foot develop compartment syndrome. Unlike other compartments, there are no classic sign of CS in the foot. The most reliable sign appears to be tense bulging tissue.

42 Forearm and Hand Fasciotomies
Compartment syndromes are less common than in the leg Supracondylar humerus fx > antebrachial compartment syndrome Anterior compartment realeased with volar incision Dorsal incision if necessary Compartment syndromes are less common in the upper extremities than in the legs. A supracondylar humerus fracture may lead to antebrachial compartment syndrome. A volar incision is made first to release the anterior compartment of the forearm including the carpal tunnel. A dorsal incision for posterior compartment decompression may be necessary. img.medscape.com/pi/emed/ckb/orthopedic_surgery/ jpg img.medscape.com/pi/emed/ckb/orthopedic_surgery/ jpg

43 Hand Fasciotomies Compartment syndrome of the hands is rare
Thenar and Hypothenar Compartment Fasciotomies Compartment syndrome of the hands is rare ? From Trauma More often iatrogenic (A-line or IV infiltrate) 10 Osseofascial Compartments Carpal tunnel release 1 or 2 dorsal incisions No sensory nerve symptoms Pressure > 20mmHg = CS jmedicalcasereports.com/content/figures/ gif Dorsal Interosseus Compartment Fasciotomies Compartment syndrome of the hand is rare, infrequently occurring due to trauma and more often due to iatrogenic factors such as an A-line or IV infiltrate. There are 10 osseofascial compartment within the hand most of which can be released with a carpal tunnel release and 1 or 2 dorsal incisions. No sensory nerves run in the compartments and so patients with compartment syndrome have no sensory symptoms. Unlike other compartments, a pressure of 20mmHg is consistent with compartment syndrome and is an indication for fasciotomies. jmedicalcasereports.com/content/figures/ jpg

44 Rhabdomyolysis Damage to skeletal muscle Crush Metabolic
Injures cells Decreases perfusion Metabolic Cell lysis due to edema Calcium in sarcoplasmic reticulum Muscle contractions Depletes ATP Damage to mitochondrion Reactive oxygen species Neutrophils migrate Increased inflammatory response Muscle compresses local structures > Compartment Syndrome > Decreased Perfusion Muscle cells release potassium, phosphate, myoglobin, creatine kinase and uric acid Rhabdomyolysis refers to the breakdown of muscle cells. It can be initiated by several different causes of muscle damage. Crush injuries damage the cells directly as well as impede perfusion. Metabolic etiologies may cause cell lysis. The inflammation due to muscle damage can further lead to cell lysis. Following cell lysis, calcium accumulates in the sarcomplasmic reticulum, causing repeated muscle contractions and depleting the cells ATP. In addition damage to the mitochondrion generates reactive oxygen species. Neutrophils migrate to the site of damage and increase the inflammatory response. The muscle as it swells compresses adjacent structures within the same compartment which results in a compartment syndrome. Perfusion is further decreased and muscle cells continue to die, releasing potassium, phosphate, myoglobin, creatine kinase and uric acid into the bloodstream.

45 Rhabdomyolysis Myoglobin Nephrotoxic Muscle swelling
Intravascular volume deficit Renal hypoperfusion Uric acid Precipitates in renal tubules Accumulates in renal tubules Rhabdomyolysis occurs when skeletal muscles are damaged and release myoglobin into the bloodstream. Myoglobin is an iron-containing pigment that can cause severe damage to the kidneys. The large mass of muscle tissue edema leads to depletion of intravascular fluid, compromising blood flow to the kidney. Uric acid precipitates in the tubules and may result in obstruction. Myoglobin accumulates in the renal tubules.

46 Rhabdomyolysis Myoglobinuria Plasma myoglobin > 1.5 mg/dL
Myoglobin casts cause nephron obstruction Urine Acidification Tea-colored urine Urine dipstick + for blood Urine – for red blood cells on microscopy Myoglobinuria occurs when the levels in plasma exceed 1.5 mg/dl. As the kidneys reabsorb more water, myoglobin casts form and obstruct the flow of fluid through the nephron. In addition , the high levels of uric acid causes acidification of the filtrate. Iron from the myoglobin generates reactive oxygen species, damaging the kidney cells. Acute tubular necrosis ensues. The kidney is rendered unable to perform filtration, electrolyte regulation, and hormone production (resulting in depletion of vitamin D and calcium). The myoglobinuria appears tea-colored. While urine dipstick appears postive for blood, microscopy reveals no red blood cells in the urine. lifeinthefastlane.com/wp-content/uploads/2009/12/image_34.jpg

47 Rhabdomyolysis Management Replete Volume Mannitol Sodium bicarbonate
Increases flushing of myoglobin from renal tubules Effective radical scavenger Sodium bicarbonate Alkalization of Urine Decreases cast formation Decreases direct toxic effect of myoglobin on the renal tubules Management of rhabdomyolysis is supportive and aimed at minimizing damage to the kidney. Volume repletion with maintainance of high urine ouput is the main goal of therapy. Mannitol has been shown in some trials to be effective, likely due to the increase in intravascular volume flushing myoglobin from the renal tubules. Mannitol is also an effective free radical scavenger, reducing damage to the nephron. Sodium bicarbonate has been used as a treatment to alkalinize urine, decreasing the deposition of myoglobin in the renal tubules, decreasing cast formation, and decreasing the toxic effects of myoglobin on the renal tubules. bioephemera.com/wp-content/uploads/2007/06/jimstanisg1.jpg

48 Myositis Ossificans Severe blunt trauma Intra-muscular hematoma
Delayed ossification of the soft tissue Suspected to be due to premature return to strenuous activity Most common sites: - arms - quadriceps • Treatment - Conservative - Rarely, surgical debridement A rare event that may occur with severe blunt trauma to the muscle results in an intra-muscular hematoma that undergoes delayed ossification of the soft tissue. Newly formed bone may even form a marrow cavity. These most commonly occur in the arms or quadriceps. They are thought to be due to a premature return to strenuous activity. Treatment is primarily conservative. Symptomatic patients occassionally require surgical debridement of the abnormal tissue.

49 Image Sources bp2.blogger.com/_OY2fM522a9Y/SBZ0DYml2xI/AAAAAAAABA4/KXVlqSv6hA8/s400/icu.gif bp3.blogger.com/_v2GFIISzHOU/SAjilu3b8kI/AAAAAAAAASk/3BRF9vWKgYY/s400/Neuro-Muscular+Junction.jpg bioephemera.com/wp-content/uploads/2007/06/jimstanisg1.jpg casesjournal.com/content/figures/ gif ccforum.com/content/figures/cc jpg dericbownds.net/uploaded_images/myoglobin.jpg download.thelancet.com/images/journalimages/ /PIIS fx1.lrg.jpg drdavis.typepad.com/.a/6a00d834525ed169e201156f86664c970c-320pi

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57 References

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