UBP 4.2 (Short Form): Trauma & Burn Flashcards

Secondary Subject -- Trauma – Initial Survey/Parkland Formula/Inhalational Injury/Carbon Monoxide Poisoning/Compartment Syndrome/Bone Cement Implantation Syndrome/Fat Embolism/ Myoglobinuria/Abdominal Compartment Syndrome

1
Q

How would you evaluate this patient?

(A 43-year-old, 6’1”, 96 kg, firefighter presents to the trauma suite as a level 1 trauma. He was trapped in a burning building when the roof collapsed, suffering burns to his arms, chest, and abdomen. His fellow firefighters pulled him out of the building after finding him with his left leg pinned under a large beam. He is currently awake and alert, with a C-collar and left leg splint in place. He says that when the roof beam fell, it hit him in the torso, knocked him down, and pinned his left leg. His medical history includes HTN, insulin dependent diabetes mellitus, and hypercholesterolemia. Vital Signs: BP = 98/62 mmHg, HR = 120, SaO2 = 98% on 6 L oxygen by face mask, RR = 22. EKG**: Sinus tachycardia)

A

My evaluation of this trauma patient would include –

an initial rapid assessment to determine whether the patient was stable, unstable, dying, or dead (a.k.a. rapid overview).

This would be quickly followed by a primary survey to assess and stabilize the patient’s airway, ventilation, circulation, and neurologic function (_A_irway, _B_reathing, _C_irculation, and _D_isability).

This primary survey would also include a quick examination of the undressed patient, to identify additional injury (Exposure).

Next, I would perform a secondary survey to systematically evaluate the patient from head-to-toe for additional injuries, and obtain radiographs, diagnostic procedures, and laboratory tests as indicated.

Finally, after initial resuscitation and operative interventions were completed, I would plan to perform a tertiary survey within the first 24 hours to identify clinically significant injuries that were missed during the initial evaluation

(i.e. reviewing pre-existing co-morbidities, the medical record, and the results of all laboratory and diagnostic testing).

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2
Q

Based on what you already know, do you have any specific concerns about this patient?

(A 43-year-old, 6’1”, 96 kg, firefighter presents to the trauma suite as a level 1 trauma. He was trapped in a burning building when the roof collapsed, suffering burns to his arms, chest, and abdomen. His fellow firefighters pulled him out of the building after finding him with his left leg pinned under a large beam. He is currently awake and alert, with a C-collar and left leg splint in place. He says that when the roof beam fell, it hit him in the torso, knocked him down, and pinned his left leg. His medical history includes HTN, insulin dependent diabetes mellitus, and hypercholesterolemia. Vital Signs: BP = 98/62 mmHg, HR = 120, SaO2 = 98% on 6 L oxygen by face mask, RR = 22. EKG: Sinus tachycardia)

A

Given this patient’s –

  • cervical collar,
  • potentially major burn injury,
  • possible inhalational injury (he was in a closed space), and
  • diabetes mellitus,

I would be considering –

  1. the potential for difficult airway management
    • (i.e. airway edema and cervical spine instability),
  2. progressive airway obstruction
    • (i.e. third-spacing of fluid contributing to airway edema, potential inhalational injury),
  3. significant hypovolemia
    • (i.e. hemorrhage, edema formation, and third-spacing of fluids),
  4. hyperglycemia
    • (diabetic, endocrine response to burn injury),
  5. hyperkalemia
    • (from tissue destruction), and
  6. carbon monoxide poisoning.

Since his leg suffered a crush injury, I would also be considering complications associated with an extremity injury, such as –

  1. deep vein thrombosis,
  2. vascular trauma
    • (indicated by pain, pulselessness, pallor, paresthesias, sepsis and/or paresis of the extremity),
  3. fat embolism,
  4. occult hemorrhage,
  5. rhabdomyolysis,
  6. sepsis, and
  7. compartment syndrome.

UBP Live Course Note – Cyanide poisoning is also possible depending on what is burning.

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3
Q

With a blood pressure of 98/62 mmHg, does he require fluid resuscitation?

(A 43-year-old, 6’1”, 96 kg, firefighter presents to the trauma suite as a level 1 trauma. He was trapped in a burning building when the roof collapsed, suffering burns to his arms, chest, and abdomen. His fellow firefighters pulled him out of the building after finding him with his left leg pinned under a large beam. He is currently awake and alert, with a C-collar and left leg splint in place. He says that when the roof beam fell, it hit him in the torso, knocked him down, and pinned his left leg. His medical history includes HTN, insulin dependent diabetes mellitus, and hypercholesterolemia. Vital Signs: BP = 98/62 mmHg, HR = 120, SaO2 = 98% on 6 L oxygen by face mask, RR = 22. EKG: Sinus tachycardia)

A

Assuming his burns comprise at least 10-15% of his total body surface area, adequate fluid resuscitation is essential to preventing hypovolemic shock.

Burn patients are at increased risk for developing shock in the first 24 hours due to burn-induced increases in permeability throughout the vascular system (particularly in injured areas), with subsequent extravasation of plasma proteins and shifting of large volumes of fluid from the intravascular to the interstitial compartment.

This intravascular deficit is exacerbated by decreases in myocardial contractility that may occur secondary to circulating myocardial depressants, decreased coronary blood flow, increased systemic vascular resistance, and/or a diminished response to catecholamines.

Moreover, occult blood loss could also be contributory.

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4
Q

How would you calculate his fluid requirements?

(A 43-year-old, 6’1”, 96 kg, firefighter presents to the trauma suite as a level 1 trauma. He was trapped in a burning building when the roof collapsed, suffering burns to his arms, chest, and abdomen. His fellow firefighters pulled him out of the building after finding him with his left leg pinned under a large beam. He is currently awake and alert, with a C-collar and left leg splint in place. He says that when the roof beam fell, it hit him in the torso, knocked him down, and pinned his left leg. His medical history includes HTN, insulin dependent diabetes mellitus, and hypercholesterolemia. Vital Signs: BP = 98/62 mmHg, HR = 120, SaO2 = 98% on 6 L oxygen by face mask, RR = 22. EKG: Sinus tachycardia)

A

While there are several formulas to guide fluid resuscitation following burn injury,

the most widely accepted is the Parkland formula,

which calls for fluid replacement with lactated Ringer’s solution

at a rate of 4 mL/kg per percentage of burned body surface area (BSA) in the first 24 hours.

Therefore, using this formula as a guideline, I would set the rate of administration to deliver half of the volume in the first 8 hours, and the other half over the next 16 hours.

Since this formula is only a guideline, and recognizing that overaggressive fluid resuscitation may lead to –

  • impaired respiration (upper airway edema, chest wall edema, pulmonary edema),
  • impaired peripheral perfusion (increased tissue pressure leading to reduced blood flow through burned areas), and
  • abdominal compartment syndrome (fluid-induced increases in intra-abdominal pressure),

I would titrate my initial fluid resuscitation to maintain –

  • urine output of 0.5 to 1 mL/kg/hour,
  • a pulse of 80-140 beats/minute,
  • a mean arterial pressure of > 60 mmHg, and
  • a base deficit < 2.

I could also use the patient’s –

  • hematocrit (increased hematocrit suggests inadequate fluid resuscitation) and
  • pulmonary artery catheter data to guide fluid management
    • (good cardiac output,
    • acceptable filling pressures, and
    • a mixed venous oxygen tension of 35-40 mmHg suggest adequate fluid resuscitation).

Clinical Note:

  • Normal mixed venous oxygen tension (PvO2) = 35-45 mmHg
  • Normal mixed venous oxygen saturation = 65-75%
  • Base Deficit:
    • < -2 = metabolic acidosis
    • -2 to +2 = normal
    • > 2 = alkalosis
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5
Q

How would you classify the extent of this patients’ burn injury?

(A 43-year-old, 6’1”, 96 kg, firefighter presents to the trauma suite as a level 1 trauma. He was trapped in a burning building when the roof collapsed, suffering burns to his arms, chest, and abdomen. His fellow firefighters pulled him out of the building after finding him with his left leg pinned under a large beam. He is currently awake and alert, with a C-collar and left leg splint in place. He says that when the roof beam fell, it hit him in the torso, knocked him down, and pinned his left leg. His medical history includes HTN, insulin dependent diabetes mellitus, and hypercholesterolemia. Vital Signs: BP = 98/62 mmHg, HR = 120, SaO2 = 98% on 6 L oxygen by face mask, RR = 22. EKG: Sinus tachycardia)

A

The patient with burns to his arms, chest, and abdomen, could have burns involving up to 36% of his total body surface area (TBSA).

This estimate of involved BSA can be made using the “rule of 9’s”, where the head and neck, each upper extremity, the chest, the abdomen, the anterior aspect of each lower extremity, and the posterior aspect of each lower extremity represent 9% BSA (this method underestimates the extent of burn injury in children).

However, in addition to the percent of involved BSA, the extent of injury is described by the depth of the burn and the presence or absence of inhalational injury.

The depth of injury is classified as:

  1. first degree, with injury limited to the epidermis;
  2. second-degree, with injury involving the epidermis and dermis;
  3. third-degree (full thickness), with complete destruction of the epidermis and dermal layers; and
  4. fourth-degree, with involvement of the muscle, fascia, and/or bone.
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6
Q

After carefully examining the patient, you determine that he has full-thickness and partial-thickness burns involving 20% of his TBSA.

Would you intubate the patient in the trauma suite?

(A 43-year-old, 6’1”, 96 kg, firefighter presents to the trauma suite as a level 1 trauma. He was trapped in a burning building when the roof collapsed, suffering burns to his arms, chest, and abdomen. His fellow firefighters pulled him out of the building after finding him with his left leg pinned under a large beam. He is currently awake and alert, with a C-collar and left leg splint in place. He says that when the roof beam fell, it hit him in the torso, knocked him down, and pinned his left leg. His medical history includes HTN, insulin dependent diabetes mellitus, and hypercholesterolemia. Vital Signs: BP = 98/62 mmHg, HR = 120, SaO2 = 98% on 6 L oxygen by face mask, RR = 22. EKG: Sinus tachycardia)

A

Assuming the proper equipment were available, I would –

immediately intubate any burn patient with hypoxemia, respiratory distress, stridor, hypercarbia, loss of consciousness, altered mental status, or massive burn injury.

Therefore, if this patient’s burn injuries consisted of third-degree (full-thickness) burns involving > 10% of his TBSA

(in adults, major burns are defined as full-thickness burns involving > 10% of TBSA or partial-thickness burns involving > 25% of TBSA),

I would – prepare to intubate him as soon as possible to reduce the risk of progressive airway edema formation and copious secretions leading to respiratory distress, complete airway obstruction, and significant apnea-induced hypoxia.

However, if his third degree burns were minimal, and I did not see any signs of inhalational injury, hypoxemia, respiratory distress, hypercarbia, or altered mental status, I could – delay immediate intubation, monitor him carefully, and avoid the potential deleterious effects of endotracheal intubation.

Before employing this strategy, I would utilize a fiberoptic bronchoscope to examine the glottic and periglottic structures and lower airways for signs of edema or inhalational injury.

I would also order an arterial blood gas (a low PaO2 is suggestive of inhalational injury) chest x-ray, and pulmonary function tests, recognizing that these studies are often normal in the immediate post-burn period (they should still be ordered to provide baseline information).

If these studies were reassuring and I decided to delay intubation, I would then follow up with repeat studies every 3-4 hours for at least 12 hours to allow for expeditious intubation should it be required.

Clinical Note:

  • A flow volume loop demonstrating a saw-toothed or flattened inspiratory flow and an extra-thoracic obstruction is suggestive of upper airway obstruction.
  • Lower airway injury is suggested by a flow volume loop demonstrating decreased expiratory flow, forced vital capacity, and pulmonary compliance, combined with increased airway resistance.
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7
Q

You determine that 15% of the patient’s injury is third-degree burns, with second-degree burns making up the other 5%. Moreover, you note that his sputum appears to be stained with carbonaceous material.

Will you intubate him now?

(A 43-year-old, 6’1”, 96 kg, firefighter presents to the trauma suite as a level 1 trauma. He was trapped in a burning building when the roof collapsed, suffering burns to his arms, chest, and abdomen. His fellow firefighters pulled him out of the building after finding him with his left leg pinned under a large beam. He is currently awake and alert, with a C-collar and left leg splint in place. He says that when the roof beam fell, it hit him in the torso, knocked him down, and pinned his left leg. His medical history includes HTN, insulin dependent diabetes mellitus, and hypercholesterolemia. Vital Signs: BP = 98/62 mmHg, HR = 120, SaO2 = 98% on 6 L oxygen by face mask, RR = 22. EKG: Sinus tachycardia)

A

Third-degree burns involving > 10% TBSA and carbonaceous material in the sputum are consistent with major burn and probably inhalational injury, respectively.

Therefore, considering the increased risk of respiratory compromise associated with these injuries, I would – begin preparing for immediate endotracheal intubation.

Given this patient’s increased risk of –

  • difficult airway management (airway edema, cervical collar in place),
  • airway obstruction (i.e. third-spacing of fluid, inhalatonal injury, aggressive fluid resuscitation),
  • aspiration (i.e. trauma, diabetes mellitus, possible recent food ingestion), and
  • neurologic damage (unable to clear cervical spine injury due to distracting pain),

I would:

  1. administer metoclopramide, an H2-blocker, and glycopyrrolate;
  2. provide 100% oxygen for several minutes;
  3. ensure adequate airway analgesia, manual in-line stabilization, and the presence of difficult airway equipment; and
  4. perform an awake fiberoptic intubation, being careful not to inflict any additional tissue trauma.

Following intubation, I would provide sedation as tolerated.

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8
Q

Do you suspect that he has suffered significant inhalational injury?

(A 43-year-old, 6’1”, 96 kg, firefighter presents to the trauma suite as a level 1 trauma. He was trapped in a burning building when the roof collapsed, suffering burns to his arms, chest, and abdomen. His fellow firefighters pulled him out of the building after finding him with his left leg pinned under a large beam. He is currently awake and alert, with a C-collar and left leg splint in place. He says that when the roof beam fell, it hit him in the torso, knocked him down, and pinned his left leg. His medical history includes HTN, insulin dependent diabetes mellitus, and hypercholesterolemia. Vital Signs: BP = 98/62 mmHg, HR = 120, SaO2 = 98% on 6 L oxygen by face mask, RR = 22. EKG: Sinus tachycardia)

A

The history of burn injury within a closed space (inside a building) combined with the presesnce of soot-stained sputum, is suggestive of inhalational injury.

Therefore, I would examine the patient for additional signs and symptoms of airway injury, such as – singed facial hair, burned mucosa, cough, stridor, hoarseness, difficulty swallowing, and/or pharyngeal edema.

Upper airway inhalational injury is concerning since it can lead to –

  • glottic and periglottic edema formation,
  • copious and thick secretions, and
  • subsequent airway obstruction.

Unfortunately, the aggressive fluid resuscitation associated with the initial management of significantly burned patients can further exacerbate airway swelling and obstruction (third-spacing of administered fluids).

Moreover, in the event of lower airway injury (although this is less likely to occur due to the efficient cooling capacity of the upper airways), the patient may experience –

  • bronchial obstruction,
  • bronchopneumonia, and
  • air trapping due to –
    • mucosal necrosis, edema formation, tissue sloughing, copious secretions, decreased surfactant, and reduced mucociliary function
  • (parenchymal lung injury usually presents on days 1-5 as ARDS).
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9
Q

Following intubation, the patient’s blood pressure drops to 86/53 mmHg.

What do you think may be the cause of this worsening hypotension?

(A 43-year-old, 6’1”, 96 kg, firefighter presents to the trauma suite as a level 1 trauma. He was trapped in a burning building when the roof collapsed, suffering burns to his arms, chest, and abdomen. His fellow firefighters pulled him out of the building after finding him with his left leg pinned under a large beam. He is currently awake and alert, with a C-collar and left leg splint in place. He says that when the roof beam fell, it hit him in the torso, knocked him down, and pinned his left leg. His medical history includes HTN, insulin dependent diabetes mellitus, and hypercholesterolemia. Vital Signs: BP = 98/62 mmHg, HR = 120, SaO2 = 98% on 6 L oxygen by face mask, RR = 22. EKG: Sinus tachycardia)

A

Given the extent of his burns and recent trauma with the roof beam, I think the most likely causes of and/or contributing factors to his hypotension include:

  1. anesthetic drugs;
  2. hemorrhagic shock (occult bleeding secondary to thoracic, abdominal, or extremity injury);
  3. neurogenic shock (cervical spinal cord injury following intubation);
  4. cardiogenic shock secondary to burn injury-induced release of myocardial depressant factors, diminished response to catecholamines, and/or myocardial ischemia;
  5. carbon monoxide poisoning, which can cause direct myocardial toxicity secondary to effects on mitochondrial function;
  6. cyanide toxicity, which can lead to cardiovascular depression and/or arrhythmias;
  7. hypovolemic shock (significant third-spacing of fluid, inadequate fluid resuscitation);
  8. vagal response to laryngoscopy;
  9. tension pneumothorax (trauma, central line placement);
  10. fat embolism (patient has a splint on his left leg); and
  11. hypothermia (i.e. aggressive fluid resuscitation with inadequately warmed fluids).
  12. I would also consider the possibility of – an allergic reaction.
  13. Finally, if blood had been administered, I would keep in mind that his hypotension may be the result of a – transfusion reaction (ABO incompatibility) or
  14. citrate intoxication (in the case of massive transfusion).
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10
Q

An arterial blood gas shows the following:

pH = 7.22, PO2 = 108 mmHg, PCO2 = 36 mmHg, and SaO2 = 98% on 6 liters O2.

What is your interpretation?

(A 43-year-old, 6’1”, 96 kg, firefighter presents to the trauma suite as a level 1 trauma. He was trapped in a burning building when the roof collapsed, suffering burns to his arms, chest, and abdomen. His fellow firefighters pulled him out of the building after finding him with his left leg pinned under a large beam. He is currently awake and alert, with a C-collar and left leg splint in place. He says that when the roof beam fell, it hit him in the torso, knocked him down, and pinned his left leg. His medical history includes HTN, insulin dependent diabetes mellitus, and hypercholesterolemia. Vital Signs: BP = 98/62 mmHg, HR = 120, SaO2 = 98% on 6 L oxygen by face mask, RR = 22. EKG: Sinus tachycardia)

A

A pH of 7.22 with a PCO2 of 36 mmHg is consistent with –

metabolic acidosis without respiratory compensation.

Potential causes of this condition in a diabetic patient following trauma and major burn injury include –

  • shock,
  • diabetic ketoacidosis,
  • hypothermia
    • (especially with rapid rewarming, which may lead to the release of accumulated metabolic products into the central circulation),
  • carbon monoxide poisoning, and
  • cyanide toxicity.

This patient’s metabolic acidosis is probably the result of one or more of these factors in combination with the increased metabolic rate and oxygen consumption associated with major burn injury.

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11
Q

Would you treat his acidosis with sodium bicarbonate?

(A 43-year-old, 6’1”, 96 kg, firefighter presents to the trauma suite as a level 1 trauma. He was trapped in a burning building when the roof collapsed, suffering burns to his arms, chest, and abdomen. His fellow firefighters pulled him out of the building after finding him with his left leg pinned under a large beam. He is currently awake and alert, with a C-collar and left leg splint in place. He says that when the roof beam fell, it hit him in the torso, knocked him down, and pinned his left leg. His medical history includes HTN, insulin dependent diabetes mellitus, and hypercholesterolemia. Vital Signs: BP = 98/62 mmHg, HR = 120, SaO2 = 98% on 6 L oxygen by face mask, RR = 22. EKG: Sinus tachycardia)

A

I would NOT administer sodium bicarbonate at this time due to the potential complications associated with the use of this drug, such as:

  1. the generation of additional CO2
    • (bicarbonate reacts with hydrogen ions to form CO2), which could then diffuse into cells resulting in worsening intracellular acidosis (a particular risk in this patient who may not eliminate CO2 as effectively secondary to pulmonary injury);
  2. left-ward shifting of the oxyhemoglobin dissociation curve
    • (resulting in impaired tissue delivery of oxygen – which may already be compromised by carbon monoxide or cyanide poisoning);
  3. the development of a hyperosmolar state secondary to an excessive sodium load; and
  4. the development of hypokalemia secondary to movement of K+ from the extracellular to the intracellular compartment
    • (while burn patients initially tend toward hyperkalemia due to tissue necrosis and hemolysis, they often develop significant hypokalemia with time secondary to the renal loss of potassium).
    • However, if his pH dropped below 7.1, I would consider sodium bicarbonate administration to prevent the dysrhythmias, hypotension, myocardial depression, and catecholamine resistance associated with severe acidosis.
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12
Q

The resident asks you if his acidosis could be the result of carbon monoxide poisoning.

What would you say?

(A 43-year-old, 6’1”, 96 kg, firefighter presents to the trauma suite as a level 1 trauma. He was trapped in a burning building when the roof collapsed, suffering burns to his arms, chest, and abdomen. His fellow firefighters pulled him out of the building after finding him with his left leg pinned under a large beam. He is currently awake and alert, with a C-collar and left leg splint in place. He says that when the roof beam fell, it hit him in the torso, knocked him down, and pinned his left leg. His medical history includes HTN, insulin dependent diabetes mellitus, and hypercholesterolemia. Vital Signs: BP = 98/62 mmHg, HR = 120, SaO2 = 98% on 6 L oxygen by face mask, RR = 22. EKG: Sinus tachycardia)

A

The development of acidosis in a patient with suspected or known smoke inhalation injury would raise my concern that he suffered from carbon monoxide poisoning.

A normal reading from a pulse oximeter that compares only two wavelengths of light (usually 960 nm and 660 nm) would not allay my concern since carboxyhemoglobin (which forms with carbon monoxide poisoning) and oxyhemoglobin exhibit identical absoprtion of light at 660 nm, potentially leading to falsely elevated readings.

Tissue hypoxia and acidosis develop with carbon monoxide poisoning for two reasons:

  1. carbon monoxide (CO) has a 200-250 fold greater affinity for hemoglobin than does oxygen (reducing the number of available sites for binding of oxygen… somewhat like anemia); and
  2. carboxyhemoglobin results in a left-ward shift in the oxyhemoglobin dissociation curve, resulting in impaired tissue delivery of oxygen (the binding of carboxyhemoglobin at one or more sites on the hemoglobin molecule increases the oxygen affinity of the remaining oxygen binding sites, impairing the delivery of oxygen to tissues).

Given my suspicion of carbon monoxide toxicity, I would –

  • administer 100% oxygen to improve oxygenation and promote the elimination of CO (decreases the 1/2 life of CO-Hg from 4-6 hours on room air to 40-90 minutes), observe the patient’s blood for the cherry-red color associated with extremely high concentrations of CO-Hb (>40%), and order a CO-Hg level.
  • If his CO-Hg level was > 30% and the delay of other emergency care were acceptable, I would consider hyperbaric oxygen treatment to further promote CO elimination (1/2 life of CO decreased to 20-30 minutes at 3 atmospheres) and to reduce the risk of the delayed neurologic sequelae associated with CO toxicity (i.e headaches, personality changes, confusion, irritability, memory loss, and motor deficits).

Clinical Notes:

  • PaO2 is a measurement of the oxygen tension in the blood (i.e. the amount of free oxygen dissolved in the plasma). Therefore, it is not affected by the amount or binding characteristics of hemoglobin (i.e. carbon monoxide). It is, rather, affected by the alveolar PO2 and the capillary-alveolar interface.
  • SaO2 is the percentage of total arterial heme binding sites saturated with oxygen. This measurement would be affected by oxygen binding to hemoglobin (i.e. carbon monoxide). This is measured by blood oximetry.
  • The SpO2 is provided by pulse-oximetry and should approximate the SaO2 under normal circumstances. Situations where this reading may be erroneous include methemoglobinemia, carboxyhemoglobinemia, severe anemia (falsely low), following the administration of certain dyes (falsely low), nail polish, excessive ambient light, poor perfusion, and motion artifact.
  • Standard blood gas analyzers derive the SaO2 from the PaO2. Therefore, using this analyzer, a patient with significant carbon monoxide poisoning may have a normal SaO2.
  • Therefore, co-oximetry is the only reliable way to assess the oxygenation status of a patient with carbon monoxide poisoning (some blood gas analyzers employ co-oximetry).
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13
Q

A member of the trauma team says she can’t feel a dorsalis pedis pulse in his left lower extremity.

A quick examination reveals a normal EKG, a blood pressure of 104/76 mmHg, a good radial pulse on both sides, and a strong dorsalis pedis pulse on the right.

What do you think may be going on?

(A 43-year-old, 6’1”, 96 kg, firefighter presents to the trauma suite as a level 1 trauma. He was trapped in a burning building when the roof collapsed, suffering burns to his arms, chest, and abdomen. His fellow firefighters pulled him out of the building after finding him with his left leg pinned under a large beam. He is currently awake and alert, with a C-collar and left leg splint in place. He says that when the roof beam fell, it hit him in the torso, knocked him down, and pinned his left leg. His medical history includes HTN, insulin dependent diabetes mellitus, and hypercholesterolemia. Vital Signs: BP = 98/62 mmHg, HR = 120, SaO2 = 98% on 6 L oxygen by face mask, RR = 22. EKG: Sinus tachycardia)

A

Given the fact that his left leg was pinned under a fallen roof beam,

I would be concerned that his pulselessness was due to –

vascular trauma or compartment syndrome in his left lower extremity.

Therefore, I would –

confirm that pulses in the extremity were weak or absent and look for other signs associated with these conditions such as –

  • pallor,
  • paresthesias, (“pins and needles” is a common description),
  • paresis (usually a late finding).

Swelling and tenseness in the affected extremity would be more suggestive of compartment syndrome.

If the diagnosis were in doubt, I would consider –

  • arteriography or transducer measurement of intra-compartmental pressures to obtain a more definitive diagnosis
    • (immediate surgery is required when the intra-compartmental pressure exceeds 30-40 mmHg or when there is < 30 mmHg difference between the intra-compartmental pressure and the diastolic blood pressure).

With either diagnosis, immediate surgical intervention is required to prevent irreversible muscle and nerve damage.

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