3. History of Present Illness:
Went to bar on Friday night, had 6 glasses of whiskey mixed with water.
Comes home and takes 8 tablets of Advil PM (at 1:30 am) to help sleep. (takes 4
tablets every night)
Next day (Saturday) she remembers being on porch smoking cigarettes. Her parents
were leaving out of town for a wedding. Her mother told her that she does not look
right and seems disoriented.
She remembers at one point, she tried to take steps but her right leg gave away and
she fell down.
Around 12:30 am Sunday morning she had excruciating pain in her right leg - calls
EMS and was brought to the ER.
She does not remember anything except for this from last 24 hours.
4. Review of Systems:
Constitutional: Weakness, Fatigue, No fever, No chills, No sweats.
Eye: No recent visual problem.
Ear/Nose/Mouth/Throat: No nasal congestion, No sore throat.
Respiratory: No shortness of breath, No cough, No wheezing.
Cardiovascular: Left lateral chest pain, No palpitations, Right leg swelling.
Gastrointestinal: Nausea, generalized abdominal cramping, No vomiting, No diarrhea, No
constipation.
Genitourinary: No urethral discharge
Hematology/Lymphatics: No bruising tendency, No bleeding tendency, No swollen lymph
glands.
Endocrine: No cold intolerance, No heat intolerance.
Immunologic: Negative.
Musculoskeletal: Right leg is swollen, painful and numb. Not able to bear weight or move
toes.
Integumentary: Negative.
Neurologic: Alert and oriented X 4.
5. Other Histories:
PMH/PSH: Bipolar disorder, Depression, Anxiety, Hypothyroidism, ADD, Sleep apnea,
Asthma, Heartburn, Gallstones s/p Cholecystectomy, Abortion x 3, last 3 years ago.
Allergies: Lamotrigine - Rash; Hydrocodone- Itching
Medications: ProAir HFA, Synthroid 137 mcg, biotin, lysine, omeprazole 20 mg
Social History: Divorced (2012), Lives with parents, Weekend alcohol use (6-7
drinks), Smokes 6-8 cigs a day (age of 16), Marijuana use every 2-3 months, No IV
drug use.
6. Physical Examination:
Vitals: Temp: 35.5, Pulse: 110 bpm, RR: 16,
SpO2 99% on RA, BP: 125/90 mmhg.
General: Alert. moderate distress. Patient
laying down in bed holding left lower ribs by
both hands.
Skin: Normal for ethnicity
Eye: Normal conjunctiva
Ears, nose, mouth, and throat: Bluish
discoloration of the lips.
Neck: No tenderness
Cardiovascular: Tachycardia, Regular
rhythm. No murmur, No JVD
Respiratory: Lungs are clear to auscultation.
respirations are non-labored.
Chest wall: Diffuse tenderness left lower ribs,
no bruises or mass.
Back: Nontender
Musculoskeletal: Severe diffuse tenderness
present on right lower leg mainly posteriorly,
Right leg 1.5 times larger than the left one,
Reduced sensation, hard in consistency, right
foot - cold to touch, pain worse with
dorsiflexion of the foot, absent plantar reflex,
no bruises, no rash, pedal pulse intact; 5 x 5
cm abrasion at the lateral side of the right
lower leg. Few abrasion at the left knee
anteriorly.
Gastrointestinal: Soft. Nontender. Non
distended. Normal bowel sounds.
Neurological: Alert and oriented to person,
place, time, and situation. No focal
neurological deficit observed.
Lymphatics: No lymphadenopathy
Psychiatric: Appropriate mood & affect
8. Imaging:
CT head without contrast - no acute intracranial abnormality
Ribs unilateral w/chest pa left – negative for fracture
Ankle complete right - normal
Knee 4 views right - normal
Pelvis AP - negative
9. Labs:
Hemogram
WBC 17.6 H
RBC 5.44 H
Hemoglobin 16.6 H
Hematocrit 49.1 H
MCV 90.3
MCH 30.5
MCHC 33.8
RDW 15.4 H
Platelet 425 H
MPV 10.3
Nucleated
RBCs
0
Differential Automated
Neutro % 82
Lymph % 11
Mono % 6
Eos % 0
Baso % 0
Immature Gran % 0.3
Neutro # 14.5 H
Lymph # 2.0
Mono # 1.0
Eos # 0.0
Baso # 0.0
General Chemistry
Sodium 140
Potassium 4.5
Chloride 99
Co2 12 L
Anion Gap 29 H
BUN 33 H
Creatinine 4.2 H
Glucose 169 H
Calcium 7.7 L
Albumin 4.6
Alk Phos 87
AST 700 H
ALT 3604 H
Bilirubin, total 0.6
Protein, total 8.2
eGFR 12 L
10. Other tests
Magnesium 2.1
Phosphorus 9.3 H
CK, Total 247916 H
HCG Negative
Urine TOX Negative
Urine Myoglobin >12700 H
Labs:
ABG
pH 7.19 H
pCO2 42
pO2 31 H
HCO3 16 L
O2 Saturation 45 L
Urinalysis - Later
Color Straw
Clarity Cloudy
Specific gravity 1.015
PH 5.0
Leukocyte esterase Trace
Nitrite Negative
Protein Negative
Glucose 1 +
Ketones Negative
Urobilinogen Normal
Bilirubin Negative
Blood 2 +
Wbc 6 – 10
Rbc 6 – 10
Bacteria few
Epithelial cells Many
13. Introduction
Compartment syndrome occurs when increased pressure within a limited space
compromises the circulation and function of the tissues within that space.
First described in 1881 by Richard Van Volkmann, a German physician - noted that
paralysis and contractures were the late sequelae of an interruption of the blood
supply to the muscles in the forearm
In 1924, it was shown that the muscle and nerve damage could be prevented by
prompt surgical decompression of the compartment.
14. Anatomy
The borders of a confined space are
often made up of bone or tissue that
offers minimal capacity to stretch.
Increase in volume within the
compartment - elevated
Intracompartmental pressure.
In the lower extremity, the most common
site is at the level of the tibia and fibula,
where 40% of compartment syndromes
occur. The lower leg has four
compartments: anterior, lateral,
superficial posterior, and deep posterior
15. Anatomy
The upper leg – 3 compartments: anterior,
posterior, and medial.
Larger size and their interconnectivity -
less predisposed to elevated tissue
pressures.
The foot and buttock region - lower
incidence of compartment syndrome.
Forearm has 3 compartments: flexor,
extensor, and mobile wad - high-risk areas
in the arm.
Hand or upper arm - less likely to develop
a compartment syndrome.
17. Pathophysiology
Muscle death and nerve damage - caused by prolonged
elevation of tissue pressures.
External forces, such as a cast or tight dressing -
compress a compartment.
Increase in the volume of a compartment that exceeds
the limits of the fascia's ability to stretch. (hemorrhage
into a compartment or edema caused by reperfusion
injury)
Any mechanism that increases the volume of blood or
tissue within the compartment - potential to cause a
compartment syndrome.
Tissue perfusion is determined by the difference
between the arterial blood pressure and the pressure of
the venous return.
As tissue pressure increases - the normal gradient
between arterial and venous pressure decreases.
Causes of Compartment Syndrome
Orthopedic Tibial fractures
Forearm fractures
Vascular Ischemic-reperfusion injury
Hemorrhage
Iatrogenic Vascular puncture in anticoagulated
patients
IV/intra-arterial drug injection
Constrictive casts
Soft tissue
injury
Prolonged limb compression
Crush injury
Burns
Hematologi
c
Hemophilia
Adverse effects of anticoagulants
(warfarin)
18. Pathophysiology
Normal pressure within a compartment is <10
mm Hg
Pressures up to 20 mm Hg - tolerated without
significant damage.
Tissue pressures exceeding 30 to 50 mm Hg -
toxic if left untreated for several hours.
Delta pressure - (Diastolic blood pressure -
Intra-compartmental pressure) >30 mm Hg is
used for diagnosis.
Some tissues are more sensitive to the ischemic
injury produced by elevated compartment
pressures.
Bone - relatively resistant to this ischemia
The muscles and nerves - most susceptible to
permanent damage
Short periods of elevated pressures - reversible
damage, whereas longer periods lead to
permanent deficits.
Tissue Survival of Ischemia
Muscle
4 hours Reversible change
6 Hours Variable damage
8 Hours Irreversible damage
Nerve
2
Hours
Loss of nerve
conduction
4
Hours
Neurapraxia
8 Irreversible damage
19. Clinical Features
History:
May occur with or without known trauma.
Hemophilia or Rhabdomyolysis can develop compartment syndrome without direct
trauma
Trauma - Crush injury or tibial fracture - symptoms usually develop within a few
hours of the injury.
Complain of severe pain in the affected compartment - may be refractory to opioids
- worsens when the muscle groups in that compartment are passively or actively
stretched.
20. Clinical Features
Physical Examination
Pain and the aggravation of pain by passive stretching of muscles - most sensitive (and
often the only) clinical findings before the onset of ischemic dysfunction in the nerves
and muscles.
When nerve conduction is affected - Numbness or dysesthesia in the sensory
distribution of the nerve. Motor nerve function may also be affected.
Because tissue pressures do not become higher than arterial pressures, the distal pulse
in the extremity will remain normal and there will not be a change in the color or warmth
of the extremity.
Squeezing or palpation of the muscle groups in the compartments will exacerbate pain.
Firmness or fullness in the affected compartment is often detected.
21. Diagnosis
Exam findings alone may be sufficient to make the
diagnosis
Direct measurement of the tissue pressures in the
compartment
To calculate the delta pressure and confirm the diagnosis
A Stryker Kit®
22. Diagnosis
The measurement of compartment pressures may be helpful in certain settings.
Obtunded patient - making clinical evaluation with suspected compartment syndrome
difficult.
Patients under anesthesia.
It is not necessary to measure compartment pressures in a clinically obvious
compartment syndrome.
Laboratory testing:
Serum CPK and myoglobin may be elevated. Urinalysis may reveal myoglobinuria.
Hemophiliacs or patients with clotting disorders need assay of coagulation parameters
and factor levels.
23. Treatment
Initial medical management
Supplemental oxygen, blood pressure support (hypotension)
Immediately remove restrictive casts or dressings.
Place the affected limbs at the level of the heart; elevation higher than the heart increases the
arteriovenous pressure gradient.
Hemophilia - replacement of factor levels
Anticoagulants - reversal or factor replacement
Surgical fasciotomy reduces intracompartmental pressure. Long incisions - in the affected
compartment and simultaneously incise adjacent compartments. Tissue edema can cause the
muscle to bulge from the incision sites.
The wounds should be initially left open and a second look procedure for debridement and
possible closure scheduled for 48 to 72 hours after the initial intervention. Ideally, definitive wound
closure is obtained within 7 to 10 days. This may require skin grafting.
24. Disease Complications
When fasciotomy is performed in a timely fashion, it can prevent death of the
muscle and nerves
If delayed - permanent neuropathy and muscle death.
Functional impairment is unlikely when compartment syndrome is diagnosed and
treated within 6 hours of its onset.
Tissue pressures that have been elevated for 24 to 48 hours may have already
caused permanent dysfunction and opening the compartments at this time may be
futile.
NOTE:
To change the image on this slide, select the picture and delete it. Then click the Pictures icon in the placeholder to insert your own image.
The kit consists of a saline-filled syringe, a manometer, and a needle with a side port. Connect the manometer between the syringe and the needle. Insert the needle into the compartment. Inject a few drops of saline to ensure that there are no air pockets and that the needle is not inserted into a tendon. The gauge gives the pressure reading in mm Hg. Check pressures twice in each compartment. Also check adjacent compartment pressures. Because pressures are highest near the injured area, obtain the measurements within 5 cm of a fracture site. Figure 278–1 demonstrates appropriate sites for pressure measurements in the lower leg, whereas Figure 278–6 shows sites for the forearm. The hands and feet have many compartments within them, all too numerous and small to easily measure. If compartment syndrome is suspected in these sites, some specialists opt for surgical intervention without documentation of elevated pressures.
NOTE:
To change the image on this slide, select the picture and delete it. Then click the Pictures icon in the placeholder to insert your own image.