MORNING REPORT - 9
AUGUST 2, 2017
Khushboo Gandhi, PGY 3
Internal Medicine Residency Program
St. Luke’s Hospital
A 37-year-old Caucasian Female Presents
with Right Leg Pain and Weakness x 1 Day
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.
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.
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.
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
Right Leg Pain, Swelling
and Weakness.
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
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
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
Compartment Syndrome and Rhabdomyolysis
Photographs taken with informed consent
COMPARTMENT SYNDROME
Khushboo Gandhi, PGY3
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.
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
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.
Anatomy
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)
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
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.
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.
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®
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.
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.
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.
Thank You!!
RHABDOMYOLYSIS
Khushboo Gandhi, PGY3
Causes
Exertion and physical trauma
Direct trauma
Crush syndrome
Prolonged pressure with coma
Electrical shock
Thermal burns
Freezing
Excessive exercise
Athletic injury
Convulsive seizures
Punitive exercise
Hereditary myopathies
Myophosphorylase deficiency
(McArdle's disease)
Carnitine palmitoyltransferase
deficiency
Acquired metabolic disorders
Hyperthyroidism
Diabetic ketoacidosis
Potassium deficiency
Phosphorus deficiency with acute
hypophosphatemia
Alcoholism
Acute hyponatremia
Hypoxia and ischemia
Carbon monoxide poisoning
Vascular occlusion
Atheromatous embolism
Compartment syndrome
Drugs
Cocaine
Ephedra compounds
Amphetamine derivatives
Statins
Lipid-lowering drugs
Infectious disorders
Bacterial
Clostridial infection
Legionella
Streptococcal infection
Staphylococcal infection
Pneumococcal pneumonia
Viral
Influenza
Coxsackie
HIV
Toxins
Snake venom
Poisonous mushrooms
Quail fed on sweet parsley seeds
Fish poisoning (Haff disease)
Miscellaneous
Malignant hyperthermia Neuroleptic
malignant syndrome

Compartment Syndrome

  • 1.
    MORNING REPORT -9 AUGUST 2, 2017 Khushboo Gandhi, PGY 3 Internal Medicine Residency Program St. Luke’s Hospital
  • 2.
    A 37-year-old CaucasianFemale Presents with Right Leg Pain and Weakness x 1 Day
  • 3.
    History of PresentIllness:  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
  • 7.
    Right Leg Pain,Swelling and Weakness.
  • 8.
    Imaging:  CT headwithout 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 RBC5.44 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 Phosphorus9.3 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
  • 11.
    Compartment Syndrome andRhabdomyolysis Photographs taken with informed consent
  • 12.
  • 13.
    Introduction  Compartment syndromeoccurs 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 bordersof 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 upperleg – 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.
  • 16.
  • 17.
    Pathophysiology  Muscle deathand 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 pressurewithin 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:  Mayoccur 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 findingsalone 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 measurementof 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 medicalmanagement  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  Whenfasciotomy 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.
  • 25.
  • 26.
  • 27.
    Causes Exertion and physicaltrauma Direct trauma Crush syndrome Prolonged pressure with coma Electrical shock Thermal burns Freezing Excessive exercise Athletic injury Convulsive seizures Punitive exercise Hereditary myopathies Myophosphorylase deficiency (McArdle's disease) Carnitine palmitoyltransferase deficiency Acquired metabolic disorders Hyperthyroidism Diabetic ketoacidosis Potassium deficiency Phosphorus deficiency with acute hypophosphatemia Alcoholism Acute hyponatremia Hypoxia and ischemia Carbon monoxide poisoning Vascular occlusion Atheromatous embolism Compartment syndrome Drugs Cocaine Ephedra compounds Amphetamine derivatives Statins Lipid-lowering drugs Infectious disorders Bacterial Clostridial infection Legionella Streptococcal infection Staphylococcal infection Pneumococcal pneumonia Viral Influenza Coxsackie HIV Toxins Snake venom Poisonous mushrooms Quail fed on sweet parsley seeds Fish poisoning (Haff disease) Miscellaneous Malignant hyperthermia Neuroleptic malignant syndrome

Editor's Notes

  • #2 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.
  • #22 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.
  • #26 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.