CASE ICM II

A 42-year-old man was found lying down at the side of the road. He was still conscious but
complains that he cannot move his legs. According to him and the people around he was hit by a
speeding sport car when crossing the road, he was hit at the left thigh but felt down in an
awkward position with his right leg. He also complains of several painful bruises on his arm, but
otherwise he was relatively fine except both of his legs. There was also small pool of blood
where he was lying down.

The people around then move him recklessly to a taxi, then send him to emergency department.
When arrived at the hospital he was losing his consciousness, the paramedics also noticed that
there is massive pool of blood in the taxi, and then he was moved to a bed. When a doctor
checking his airway and breathing, which was okay, a nurse taking his vital signs which shows
BP 70/50 mmHg, HR 120 beat/min, RR 24 breath/min. On the exposure of the wound they found
open fracture on left thigh with pulsating bleeding and weird position of the right lower leg
below the knee. The doctor tries to stop the bleeding with arterial clamp then gives him 2 liters
of ringer lactate fast infusion via two site IV access with large-bore, short-needle IV set. X-ray of
the left thigh and right knee are obtained which shows: (attachment 1). The doctor also tries to do
closed reduction to the right leg which is successful. After the initial infusion, his vital signs just
slightly improve to BP 90/60 mmHg, HR 112 beat/min, RR 10 breath/min, so the doctor decide
to give another 2 liters of ringer lactate fast infusion while waiting for the orthopedic and
vascular surgeon.

He was the brought to operating room to have open reduction internal fixation and vascular
repair of the left thigh and also casting for his right knee. The operation went well, and he was
transferred to trauma ward. On the fourth day of treatment he complains of extreme pain and
feeling of tense on his right foot, he felt the pain since 2 days ago but he think it’s normal
because of the injury so he didn’t told the doctor. The examination shows extreme pain worsen
by extending the foot, pallor on his right lower leg, paresthesia, loss of digital motion, deficit
pulse on right dorsalis pedis artery. Complete blood and urine lab exam was obtained and the
result shows:

Blood: SGOT 52 U/L

SGPT 40 U/L

            Potassium 7,2 mEq/L

Phosphate 6,0 mEq/L

Calcium 6,0 mg/dL

Uric acid 10,1 mg/dL

CK serum level 10.000 IU/L

PT / APTT within normal limits

Urine: Brown colored urine

Dipstick blood (+)

Urine sediment RBC (-)

He was treated with bicarbonate and Ringer lactate 500 mL/hour, and then titrated to maintain
his urine output 300 mL/hour. The orthopedic surgeon then performs fasciotomy on his right
lower leg. The vascular surgeon then assess his right popliteal artery and found thrombosis and
decide to do arterial reconstruction on the. site of thrombus After several days his condition is
improved and then he was discharged after 10 days of treatment.

1. What are his problems?

Main Problems:
1. Cannot move his legs (berarti keduanya)
2. Left leg was hit by Car (left leg) and felt down with right leg in abnormal position
3. Several painful bruises on his arm
4. Small pool of blood (ada hemorrhage) Then massive pool of blood at taxi (makin
parah),
5. Loss of Consciousness when in ED → curiga karena massive blood loss,
hemorrhagic shock
Pemeriksaan Fisik
 Airway and breathing Normal
 BP 70/50 (blood loss), HR 120x/mins (kompensasi), RR 24x/mins (kompensasi)
→ kompensasi biar blood tetap sampai ke vital organs (brain, kidney, lung) dan tidak
hypoxia
 Open fracture on left thigh with pulsating bleeding (active hemorrhage)
 Weird position of right lower leg → curiga closed fracture atau subluxation  or
dislocation
Next Treatment
 Bicarbonate → biasanya buat treat metabolic acidosis, nambah cairan
 RL 500 mL/h (maintain urine output 300 mL/h) → tambah cairan jg
 Fasciotomy di right lower leg, ditemukan juga ada thrombosis , dilakukan reconstruction
di site of thrombus

Initial Treatment (dari kasus) → → → → → → → → → → → → → → 

 Memberhentikan bleeding dengan arterial clamp.
 Diberikan 2 Liter IV RL, 2 site with fast infusion, large bore, short needle IV set (untuk
daerah perifer pakai short/midline needle) → biasanya 20 ml/kgBB
 Close reduction (tutup luka)
 Hasil dari initial tx: BP 90/60, HR 112x/mins, RR 10x/mins, kemudian diberikan
tambahan 2 Liter IV RL fast infusion, rujuk ortopedi & bedah vascular
 Dilakukan ORIF (Open Reduction Internal Fixation) & vascular repair → berhasil

o 2 hari kemudian terdapat extreme pain, feeling of tense on his right foot, baru bilang
di hari ke 4
o Extreme pain when extending foot, pallor on his lower leg, paresthesia, loss of
digital motion, deficit pulse on dorsalis pedis artery dextra.

2. interpret lab results

Pemeriksaan Lab
 OT / PT = 52 / 40 → increase / normal---
 Potassium (kalium) = 7,2 mEq/L (increase)
 Phosphate = 6,0 mEq/L (entah typo atau gimana, kalau pakai satuan aslinya mg/dL dgn
normal value 2.0-4.5 mf/dL, jadi setelah di konversi 9.3 mg/dL, cmiiw)
 Ca = 6,0 mg/dL (decrease)
 Uric acid = 10,1 mg/dL (Increase)
 CK serum level = 10.000 IU/L (indicate MSK damage and or other cells, increase)
 PT/APTT = normal
 Urine interpretation = brown coloured (+CK 10,000 U/L → curiga rhabdomyolysis),
dipstick blood (+), sedimen rbc(-)

3. Interpret radiology findings

 Nampak Comminuted Fracture di Media Femur Sinistra

 Nampak Dislocation ke arah Anteromedial (tibia) dari FemuroTibial joint

4. Closed reduction techniques

5. ORIF technique (gak perlu terlalu dalam pembahasannya)
 6. Diagnose this patient’s condition
a. before and after closed reduction

About the Procedure

The procedure is often painful. You will receive medicine to block the pain during the procedure. You
might receive:

A local anesthetic or nerve block to numb the area (usually given as a shot)
A sedative to make you relaxed but not asleep (usually given through an IV, or intravenous line)
General anesthesia to make you sleep during the procedure
After you receive pain medicine, your provider will set the bone in the right position by pushing or
pulling the bone. This is called traction.

After the bone is set:

You will have an x-ray to make sure the bone is in the right position.
A cast or splint will be put on your limb to keep the bone in the right position and protect it while it heals.

After Your Procedure

If you do not have other injuries or problems, you will be able to go home a few hours after the
procedure.

Until your provider advises, do not:

Place rings on your fingers or toes over your injured arm or leg
Bear weight on the injured leg or arm

b. After ORIF —> why he complains extreme pain

Pembahasan Kasus
Type of Fracture
 Displaced Fracture: bone breaks into two or more pieces and moves out of alignment.
 Non-Displaced Fracture: the bone breaks but does not move out of alignment.
 Closed Fracture: the skin is not broken.
 Open Fracture: the bone has broken through the skin 
 Avulsion Fracture: when a fragment of bone is separated from the main mass.
 Buckled Fracture: (or impacted fracture), ends are driven into each other;
commonly seen in arm fractures in children.
 Comminuted Fracture: the bone breaks into several pieces.
 Compression or Wedge Fracture: usually involves the bones in the back
(vertebrae).
 Greenstick Fracture: an incomplete fracture in which the bone is bent; occurs
most often in children.
 Linear Fracture: the break is parallel to the bone’s long axis.
 Oblique Fracture: the break has a curved or sloped pattern.
 Pathologic Fracture: caused by a disease that weakens the bones.
 Spiral Fracture: one part of the bone has been twisted at the break point.
 Stress Fracture: a hairline crack.
 Transverse Fracture: the broken piece of bone is at a right angle to the bone’s
axis.
Type of Femorotibial Joint dislocation
1. Posterior: due to an anterior-to-posterior blow to the proximal tibia
2. Anterior: due to hyperextension of the knee. Research has shown that approximately 30
degrees of hyperextension is needed to cause dislocation (Medscape).
3. Medial: due to a valgus force applied to the proximal tibia.
4. Lateral: due to a varus force applied to the proximal tibia.
5. Rotatory: generally due to an indirect rotatory force where the body rotates in the
opposite direction of a planted food. Subdivisions of rotatory dislocation include:
anteromedial, anterolateral, posteromedial, posterolateral.

Management for Major Arterial Hemorrhage

1. Apply dressing pressure (w/wo Elastic bandage)
2. If bleeding persist , apply manual pressure at proximal artery of injury. Consider
using Manual Tourniquet / Pneumatic Tourniquete (250mmHg for Upper limb and
400mmHg for Lower limb) to the proximal artery. Ensure time of tourniquet
documented. Remember: The risk of tourniquet (e.g. Compartment Syndrome) increase
 within time. If tourniquet must remain in place for prolonged period, the choice of save a
life over limb should be made.
3. Immediately consult to surgeon skilled in vascular and extremity trauma.
4. Apply vascular clamp to the open wound bleeding (not recommended unless superficial
artery is clearly identified)
5. If a fracture is associated with an open hemorrhaging wound, realign and splint it while
a second person applies direct pressure to the open wound. 
6. Joint dislocations should be reduced, if possible; if the joint cannot be reduced,
emergency orthopedic intervention may be required
7. Amputation (not recommended due to emotional pain, except for lifesaving and inform
consent) → due to prolonged ischaemia, nerve injury, muscle damage
8. Replantation if possible→ reattachment part of body, not recommended if px with
multiple injury that needs intensive resuscitation.

Management for Fracture

1. Assessment for pain, swelling, deformity, crepitus, abnormal motion at fracture site
2. Initial treatment is immobilization to reduce complication. Positioning to re-align as
close as anatomical position. Proper splint useful for control blood loss, reduce pain,
prevent neurovascular compromise and soft tissue injury.
3. Assess for Neurovascular status (pulse/vascularization, tingling/paraeshtesia or
hypoesthesia, etc.)
4. Apply traction (advanced only!) complication from traction is neurovascular injury!
5. If open fracture is exist, pull the exposed bone back into the wound (for advanced
only) → needs surgical debridement to prevent Osteomyelitis. Remove gross
contamination and particulate matter within the wound. And administer IV
antibiotics weight-based dosage (with First generation of cephalosporin (e.g
cefazolin, cephalothin); if Penicillin allergy and besides using 1st gen cephalosporin
(Clindamycin); if gram negative (Gentamicin); Gram negative and positive coverage
(Piperacilin/Tazobactam).
6. Operative revascularization to restore arterial blood flow to an ischaemic extremity. CT
angiography for vascular evaluation
7. Bone Fixation using ORIF / OREF (Open Reduction Internal / External Fixation) → not
from ATLS, otherwise from this, are from ATLS.

Management Compartment Syndrome

Assess for:
 Pain greater than expected and out of proportion to the stimulus or injury
 Pain on passive stretch of the affected muscle
 Tense swelling of the affected compartment
 Paresthesias or altered sensation distal to the affected compartment
Treatment is only Fasciotomy (open surgery to reduce pressure)
Peripheral vascular injury :

1. Patof

2. Clinical manif based on

2a. history

2b. physical

3. Causes

4. Lab

5. Imaging

6. Treatment:

6a. Prehospital

B. Emergency department care

7. Follow up for

a. Inpatient care

B. Outpatient care

8. Complications

9. Prognosis

10. Patient education

Referral to specialist apa

COMPARTMENT SYNDROME : Compartment syndrome is a painful condition that occurs when

pressure within the muscles builds to dangerous levels. This pressure can decrease blood flow,
which prevents nourishment and oxygen from reaching nerve and muscle cells.

1. Patof

Acute compartment syndrome occurs due to decreased intracompartmental space or increased

intracompartmental fluid volume because the surrounding fascia is inherently non-compliant. As
the compartment pressure increases, hemodynamics are impaired. There is normally an
equilibrium between venous outflow and arterial inflow. When there is an increase in
compartmental pressure, there is a reduction in venous outflow. This causes venous pressure and,
thus, venous capillary pressure to increase. If the intracompartmental pressure becomes higher
than arterial pressure, a decrease in arterial inflow will also occur. The reduction of venous
outflow and arterial inflow result in decreased oxygenation of tissues causing ischemia. If the
deficit of oxygenation becomes high enough, irreversible necrosis may occur.
The normal pressure within a compartment is less than 10 mmHg. If the intracompartmental
pressure reaches 30 mmHg or greater, acute compartment syndrome is present. However, a
single normal ICP reading does not exclude acute compartment syndrome. ICP should be
monitored serially or continuously.
2. Clinical manif based on

2a. history

Acute compartment syndrome typically occurs within a few hours of inciting trauma. However,
it can present up to 48 hours after. The earliest objective physical finding is the tense, or ''wood-
like" feeling of the involved compartment. Pain is typically severe, out of proportion to the
injury. Early on, pain may only be present with passive stretching. However, this symptom may
be absent in advanced acute compartment syndrome. In the initial stages, pain may be
characterized as a burning sensation or as a deep ache of the involved compartment. Paresthesia,
hypoesthesia, or poorly localized deep muscular pain may also be present.
Classically, the presentation of acute compartment syndrome has been remembered by "The Five
P's": pain, pulselessness, paresthesia, paralysis, and pallor. However, aside from paresthesia,
which may occur earlier in the course of the condition, these are typically late findings. Beware
that the presence or absence of a palpable arterial pulse may not accurately indicate relative
tissue pressure or predict the risk for compartment syndrome. In some patients, a pulse is still
present, even in a severely compromised extremity. 

 A new and persistent deep ache in an arm or leg

 Pain that seems greater than expected for the severity of the injury
 Numbness, pins-and-needles, or electricity-like pain in the limb
 Swelling, tightness and bruising

Chronic exertional compartment syndrome is an exercise-induced muscle and nerve condition that
causes pain, swelling and sometimes disability in the affected muscles of the legs or arms.

Signs and symptoms can include:

 Aching, burning or cramping pain in a compartment of the affected limb

 Tightness in the affected limb

 Numbness or tingling in the affected limb

 Weakness of the affected limb, Difficulty moving the foot

 Foot drop, in severe cases, if legs are affected

 Occasionally, swelling or bulging as a result of a muscle hernia

Pain caused by chronic exertional compartment syndrome typically follows this pattern:

 Begins consistently after a certain time, distance or intensity of exertion after you start
exercising the affected limb

 Progressively worsens as you exercise

 Becomes less intense or stops completely within 15 minutes of stopping the activity

 Over time, recovery time after exercise may increase

2b. physical

Physical exam should focus on the neurovascular territory of the involved compartment:

 Observe skin for lesions, swelling, or color change
 Palpate over the compartment, observing temperature, tension, tenderness
 Check pulses
 Evaluate two-point discrimination and sensation
 Evaluate motor function
Although the clinical features discussed above can help identify compartment syndrome, they
have limited sensitivity and specificity. Other factors, such as compartment pressures, can help
make the diagnosis.
3. Causes

Acute compartment syndrome

Acute compartment syndrome can be caused by:

 a broken bone or a crush injury – this is the most common cause 

 a plaster cast or tight bandage being applied to a limb before it has stopped swelling 
 burns, which can cause the skin to become scarred and tight 
 surgery to repair a damaged or blocked blood vessel (once blood is able to flow back into a
muscle, it can lead to swelling) 
In rare cases, it can occur without any obvious injury.

Acute compartment syndrome can occur with any condition that restricts the intracompartmental
space or increases the fluid volume in the intracompartmental space. Acute compartment
syndrome can occur without any precipitating trauma but typically occurs after a long bone
fracture, with tibial fractures being the most common cause of the condition, followed by distal
radius fractures. Seventy-five percent of cases of acute compartment syndrome are associated
with fractures. After fractures, the most common cause of acute compartment syndrome is soft
tissue injuries. Other causes of acute compartment syndrome include burns, vascular injuries,
crush injuries, drug overdoses, reperfusion injuries, thrombosis, bleeding disorders, infections,
improperly placed casts or splints, tight circumferential bandages, penetrating trauma, intense
athletic activity, and poor positioning during surgery. 
In children, supracondylar fractures of the humerus and both ulnar and radial forearm fractures
are associated with compartment syndrome.
Chronic compartment syndrome : usually occurs in young people who do regular repetitive exercise,
such as running, biking, or swimming, cycling. The exact cause is unknown. A leading theory is that it's
caused by temporary swelling of the muscles during exercise affecting the blood supply to a whole group
of muscles.

4. Lab

 Radiographs should be obtained if a fracture is suspected

 Measurement of intracompartmental pressure is not required but can aid in diagnosis if
uncertainty exists. Compartment pressures are often measured with a manometer, a
device that detects intracompartmental pressure by measuring the resistance that
is present when a saline solution is injected into the compartment. Another method
employs a slit catheter, whereby a catheter is placed within the compartment, and the
pressure measured with an arterial line transducer. The slit catheter method is more
accurate and allows for continuous monitoring. Its use is also recommended to measure
all the surrounding compartments.
o The normal pressure within the compartment is between 0 mmHg to 8 mmHg.
o An intra-compartmental pressure greater than 30 mmHg indicates
compartment syndrome and a need for fasciotomy.[20]
o When intra-compartmental pressure increases to within 10 mmHg to 30 mmHg of
the patient's diastolic blood pressure, this indicates inadequate perfusion and
relative ischemia of the involved extremity.
o The perfusion pressure  of a compartment, also known as the compartment delta
pressure, is defined as the difference between the diastolic blood pressure and the
intra-compartmental pressure:
 delta pressure = diastolic pressure - measured intracompartmental pressure
 clinicians often utilize delta pressure less than or equal to 30 mmHg as
indicative of the need for fasciotomy.
 Ultrasound with Doppler can be used to look for occlusion or thrombus.
 Elevations in creatine phosphokinase (CPK) may suggest muscle breakdown from
ischemia, damage, or rhabdomyolysis.
o If rhabdomyolysis is being considered, renal function tests, urine myoglobin, and
urinalysis should be done.
o If rhabdomyolysis is diagnosed, a chemistry panel is needed.
  Preoperative studies should, at a minimum, include a complete blood count and
coagulation studies

To confirm chronic compartment syndrome, your doctor will measure the pressures in your
compartment before and after exercise. If pressures remain high after exercise, you have chronic
compartment syndrome

5. Imaging :

compartment syndrome of leg

 CT (figure 2a) and MRI (figure 2b-2e) of the left leg show pancompartmental muscular atrophy (straight
white arrow), fibrosis with focal calcification (black arrow, low signal lesions on T1 and T2 weighted
images). Circumferential subcutaneous soft tissue swelling (curved arrow) is consistent with clinical
diagnosis of cellulitis. a. CT without contrast enhancement b. T1-weighted image, TR/TE: 506/8 c. T2-
weighted image, TR/TE: 4300/102 d. T1-weighted image with fat-suppression, TR/TE: 656/8 e. T2-
weighted image, TR/TE: 4532/86
Figure 1. MRI of the right leg, case 1, was performed after fasciotomy and showed pancompartmental
muscular swelling (1a: muscular swelling with obliteration of intermuscular fat planes on the T1-
weighted image), interstitial hemorrhage (thin black arrow in 1c: high-signal regions on T1-weighted
images with fat-suppression), and edema (open arrow in 1b: highsignal regions on T2-weighted images).
Post Gd-enhanced images show localized patchy enhancement and focal myonecrosis (arrowheads in
1d: non-enhancing muscles surrounded by rim enhancement concluded as myonecrosis). Note that the
lesions are confined in the right lower leg with pancompartmental and continuous involvement without
skip lesions. a. T1-weighted image, TR (repetition time)/TE (echo time): 506/7 b. T2-weighted image,
TR/TE: 4540/85 c. T1-weighted image with fat-suppression, TR/TE: 623/7 d. Post Gd-contrast T1-
weighted image with fat-suppression, TR/TE: 623/7 e. Post Gd-contrast T1-weighted image with fat-
suppression, TR/TE: 629/7
2.a 2b

2c
The axial T1-weighted image (2A) demonstrates slight volume increase in the lateral compartment
musculature with lateral bowing of the overlying fascia (arrowheads). Areas of diffuse T1 hyperintensity
reflect regions of hemorrhage within the muscles (arrows). The more proximal of the axial T2-weighted
images (2B) demonstrates diffuse swelling and edema-like signal throughout the lateral compartment
(arrows). The fascia is bowed laterally and may be slightly thickened (arrowheads). In addition, edema-
like signal is seen adjacent to the fascia within the subcutaneous fat. A more distal T2-weighted image
(2C) demonstrates similar findings with more pronounced soft tissue edema and a small fibular fatigue
fracture (arrow).
Diagnosis : Acute compartment syndrome involving the lateral compartment of the right leg associated
with a fibular fatigue fracture.

A B
C D
Figure 4:
Images from an MR examination of the left leg obtained on a 45 year-old male with pain in the proximal
to mid portions of the leg. The axial T1-weighted image (4A) suggests slight bowing of the fascia over the
anterior and lateral compartments. However, in this muscular individual with a limited amount of
subcutaneous fat, this is uncertain. No intramuscular hemorrhage is identified. The axial fat suppressed
proton-density weighted image (4B) demonstrates increased signal within the anterior compartment
(red asterisk) and less pronounced signal increase in the lateral compartment (blue asterisk). Coronal fat
suppressed T2-weighted images through the anterior (4C) and lateral (4D) compartments confirm the
findings (arrows). The findings are compatible with chronic exertional compartment syndrome involving
the anterior and lateral compartments of the leg.

Bulging and T2 hyperintensity may also be seen in the adjacent fascia [Figures 1, 5]. Other MR imaging
findings observed in the setting of acute and chronic compartment syndrome include the
following: 14,16,17
  Increased signal intensity on fat-suppressed T2-weighted images resulting from increased
interstitial water or edema (Figures 1, 4) (acute or chronic compartment syndrome)
 Increased signal intensity on T1-weighted images indicating foci of hemorrhage (Figures 1, 5, 6)
(acute compartment syndrome) or fatty infiltration (sequela of established compartment
syndrome)
 Decreased signal intensity on T1-weighted images caused by fibrosis or dystrophic calcification
(Figure 7) (sequela of established compartment syndrome)
 Increased muscle volume caused by muscle hypertrophy, swelling, or both (Figures 1, 5, 6)
(acute or chronic compartment syndrome)
 Decreased muscle volume related to atrophy, fibrosis, or both (sequela of established
compartment syndrome)
 Fascial thickening (Figures 1, 6) (sequela of established compartment syndrome)
 Herniation of muscle through a tear in the surrounding fascia (Figure 8) (acute or chronic
compartment syndrome)

6. Treatment:

Acute compartment syndrome must be treated in hospital using a surgical procedure called an
emergency fasciotomy. The doctor or surgeon makes an incision to cut open your skin and fascia
surrounding the muscles to immediately relieve the pressure inside the muscle compartment. The
wound will usually be closed a few days later. Occasionally, a skin graft may be required to cover the
wound.

Acute compartment syndrome is an emergency condition. Less time should be spent on

confirmation of the diagnosis, as delayed treatment may result in loss of limb.
 Immediate surgical consult
 Provide supplemental oxygen.
 Remove any restrictive casts, dressings, or bandages to relieve pressure.
 Keep the extremity at the level of the heart to prevent hypo-perfusion.
 Prevent hypotension and provide blood pressure support in patients with hypotension.
 If ICP greater than or equal to 30 mmHg or delta pressure less than or equal to
30mmHg, fasciotomy should be done.
For patients who do not meet diagnostic criteria for acute compartment syndrome but who are at
high risk based on history and physical exam findings, or for patients with intracompartmental
pressures between 15 to 20 mmHg, serial intracompartmental pressure measurements are
recommended. Patients with ICPs between 20-30 mmHg should be admitted and the surgical
team should be consulted. For patients with intracompartmental pressures greater than 30 mmHg
or delta pressures less than 30 mmHg, surgical fasciotomy should be done.
Acute compartment syndrome is a surgical emergency, so prompt diagnosis and treatment are
critical. Once the diagnosis is confirmed, immediate surgical fasciotomy is needed to reduce the
intracompartmental pressure. The ideal timeframe for fasciotomy is within six hours of injury,
and fasciotomy is not recommended after 36 hours following injury. When tissue pressure
remains elevated for that amount of time, irreversible damage may occur, and fasciotomy may
not be beneficial in this situation.
If necrosis occurs before fasciotomy is performed, there is a high likelihood of infection which
may require amputation. If infection occurs, debridement is necessary to prevent systemic spread
or other complications.
After a fasciotomy is performed and swelling dissipates, a skin graft is commonly used for
incision closure. Patients must be closely monitored for complications which include infection,
acute renal failure, and rhabdomyolysis.

Postoperative and Rehabilitation Care

 Physical therapy to regain function and strength and prevent contractures and stiffness.
 Wound care and monitoring for any ischemia, infection, gangrene.
 Antibiotics if infection if warranted 
 Pain medicine 
 The patient will need to learn how to use an ambulatory device like crutches until healing
is complete.
 An occupational therapy consult is recommended to help teach the patient how to
perform daily living activities

Consultations
Management of acute compartment syndrome involves a multidisciplinary approach. Initially,
the patient is attended to by a general or orthopedic surgeon. Depending on the complications,
the following may be consulted in the management of patients with acute compartment
syndrome:
 Infectious disease
 Wound care
 Physical therapy
 Occupational therapy

Chronic compartment syndrome is not usually dangerous, and can sometimes be relieved by stopping
the exercise that triggers it and switching to a less strenuous activity.

Physiotherapy, shoe inserts (orthotics) and non-steroidal anti-inflammatory medicines may help – speak

to your GP about this. Surgery will only be considered if your symptoms persist despite these measures.
In these cases, you'll go on a waiting list, as chronic compartment syndrome is not a medical emergency.

Exertional compartment syndrome usually goes away if you stop exercising. But you should still discuss
it with your healthcare provider. Your provider may recommend:

 Anti-inflammatory medications like non-steroidal anti-inflammatory drugs (NSAIDs).

 Cross-training (mixing up exercise types, instead of doing the same thing over and over).
 Low-impact exercise.
  Orthotics (inserts for your shoes).
 Physical therapy.
 Softer surfaces for workouts (running on tracks instead of concrete, for example).

6a. Prehospital

B. Emergency department care

7. Referral to specialist apa : ortopedi surgeon, sp bedah

RHABDOMYOLISIS : Rhabdomyolysis adalah suatu sindrom atau kumpulan gejala yang disebabkan oleh
kerusakan dan kematian jaringan otot rangka. Sindrom ini terjadi akibat rusaknya serat-serat otot dan
keluarnya isi serat tersebut ke dalam aliran darah.

1. Patof
While the etiology of a specific case of rhabdomyolysis is often known, the exact pathways
by which the various insults that can cause this syndrome ultimately lead to muscle injury
and necrosis are less clear. Much clearer is the picture of the final common events shared by
the diverse etiologies of rhabdomyolysis. Irrespective of the initial insult, the final steps
leading to rhabdomyolysis involve either direct myocyte injury or a failure of the energy
supply within the muscle cells.16
During normal muscle physiology at rest, ion channels (including Na +/K+ pumps and
Na+/Ca2+ exchangers) located on the plasma membrane (sarcolemma) maintain low
intracellular Na+ and Ca2+concentrations and high K+ concentrations within the muscle fiber.
Muscle depolarization results in an influx of Ca2+ from the reserves stored in the sarcoplasmic
reticulum into the cytoplasm (sarcoplasm), causing the muscle cells to contract through actin-
myosin cross-linking. All of these processes are dependent on the availability of sufficient
energy in the form of adenosine triphosphate (ATP). Therefore, any insult that damages the
ion channels through direct myocyte injury or reduces the availability of ATP for energy will
cause a disruption in the proper balance of intracellular electrolyte concentrations.
When muscle injury or ATP depletion occurs, the result is an excessive intracellular influx of
Na+ and Ca2+. An increase in intracellular Na+draws water into the cell and disrupts the
integrity of the intracellular space. The prolonged presence of high Ca2+ levels intracellularly
leads to a sustained myofibrillar contraction that further depletes ATP.16 Also, the elevation in
Ca2+ activates Ca2+-dependent proteases and phospholipases, promoting lysis of the cellular
membrane and further damage to the ion channels. 1 The end result of these alterations within
the muscle cell milieu is an inflammatory, self-sustaining myolytic cascade that causes
necrosis of the muscle fibers and releases the muscle contents into the extracellular space and
the bloodstream.10 Figure 1illustrates this process, showing how a wide array of insults can
ultimately coalesce upon a final common effector pathway to initiate the rhabdomyolysis
cascade.
2. Clinical manif based on

2a. history : tanyain gejala yg mungkin muncul dri penyakit ini, r.penyakit, (Socrates)

Examine you and ask about recent physical activity, prescription medications, and alcohol or drug use.
The physician must have a high index of suspicion and a thorough history and physical examination to
accurately diagnose rhabdomyolysis. With the classic triad being observed in only <10% of patients, any
patient with known risk factors––including trauma, sepsis, muscular disease, and immobilization––
should be suspected for rhabdomyolysis.

Gejala yang muncul cenderung mencerminkan primary disease process, serta superimposed symptoms
of renal failure or muscle injury. Trias klasik gejala rhabdomyolysis terdiri dari mialgia, kelemahan otot,
tender and sore muscles, dan urin berwarna teh. Massa otot pasien (ada muscle swelling ga?),
konsentrasi urin, dan fungsi glomerulus dapat mempengaruhi warna urin. Gejala umum dari
rhabdomyolysis pediatrik , terlepas dari cedera ginjal, adalah nyeri otot, demam, dan prodromes virus.

2b. physical : keadaan umum,gcs, ttv, inpeksi general, neuro mascular exam

Other indirect clues include the presence of muscle injury with an unexpected rise in serum phosphate
or aspartate transaminase. A neuromuscular examination focusing on the extremities can also give
important physical clues. Color, pulse, sensation, muscle power, and size are all informative, even in
nonverbalizing patients. Bisa ada tense and swollen muscles on examination. Trias klasik diamati pada
<10% pasien saja, dan> 50% pasien tidak mengeluh nyeri atau kelemahan otot. Manifestasi sistemik yg
mungkin termasuk takikardia, malaise umum, demam, dan mual dan muntah dan karena itu tidak
spesifik. Manifestasi klinis ARF, koagulasi intravaskular diseminata, dan kegagalan multiorgan
selanjutnya dapat muncul.

3. Causes

Physical and Nonphysical Causes of Rhabdomyolysis

Drugs and Other Agents That Can Cause Rhabdomyolysis

Proposed Risk Factors for Statin-Induced Rhabdomyolysis

4. Lab : cbc (urea kreatinin), CK, urinalysis/dipstick (ada myoglobulin ga?), muscle biopsy
The gold standard for laboratory diagnosis is the determination of plasma CK. Although a cutoff
threshold has not been established, a concentration 5 times the upper limit of the normal reference
range (ie, 1,000 IU/L) is commonly used.2 CK level is generally considered predictive of the likelihood
of developing ARF(acute renal failure), and a concentration >5,000 IU/L is closely related to the
development of kidney damage. CK has a half-life of 1.5 days. As a consequence, CK blood levels
remain increased longer than the concentration of myoglobin that has a half-life of 2-4 hours.
Myoglobin concentrations tend to normalize within 6-8 hours following the muscle injury.2 Plasma
myoglobin is not as sensitive as CK for diagnosis because of its short half-life, resulting in false-
 negative tests.16 Urine myoglobin will show erythrocyte positivity on urine dipstick because the
orthotoluidine portion of the dipstick turns blue in the presence of myoglobin.
5. Treatment:
a. Prehospital
Edukasi,

Penanganan rhabdomyolysis akan diberikan sesuai dengan penyebab serta tingkat keparahannya.
Umumnya, pengobatan yang dilakukan untuk menangani rhapdomyolysis, meliputi:

 Pemberian cairan infus

Mencukupkan cairan dengan pemberian cairan melalui infus merupakan penanganan
pertama untuk membantu protein mioglobin keluar dari ginjal dan mencegah terjadinya
gagal ginjal.

 Pemberian obat
Dokter akan meresepkan obat-obatan, seperti bikarbonat dan diuretik, untuk membantu
fungsi ginjal dan menjaga keseimbangan elekrolit di dalam tubuh.

 Cuci darah (hemodialisis)

Jika ginjal telah mengalami kerusakan dan gagal ginjal akut mulai terjadi, maka prosedur cuci
darah perlu dilakukan untuk membantu fungsi ginjal.

 Operasi
Operasi fasiotomi akan dilakukan untuk menurunkan tekanan dan melancarkan sirkulasi
darah pada pasien yang mengalami sindrom kompartemen. Operasi perlu dilakukan karena
sindrom ini berisiko merusak saraf dan otot.

Jika rhabdomyolisis muncul setelah penggunaan obat-obatan tertentu, penanganan dilakukan

dengan menghentikan penggunaan obat dan menggantinya dengan obat lainnya. Pada kasus yang
berat, penderita rhabdomyolisis akan menjalani perawatan intensif untuk memonitor kondisinya.
Peluang kesembuhan rhabdomyolysis tergantung dari penyebab dan seberapa cepat
rhabdomyolysis ditangani. Tingkat kesembuhan pasien akan semakin tinggi jika pengobatan
dilakukan sedini mungkin.
b. Emergency department care
6. Referral to specialist apa : bedah syaraf, syaraf, ortopedi
7. Komplikasi