Case Report

This 21 year old, male Yemeni, weighing 89.0 kg was brought to the Accident and Emergency Department by RED CRESCENT after sustaining multiple injuries in a road traffic accident between two cars coming at high speed in opposite directions. The primary injuries were

1. Superficial laceration on forehead 3x4 cm.

2. Two longitudinal parallel burses on right 5th and 6th ribs anteriorly each measuring 2x4 cm .

3. Swelling of left mid thigh.

4. Open wound measuring 5x5cm on right lower leg with exposed tibia and fibula.

The patient was thoroughly evaluated by Surgical Trauma Team and management started accordingly.

On arrival, the patient was fully awake and well oriented in time, space and person. There was no sign of airway obstruction. He had history of momentary loss of consciousness for 5 minutes at the scene. He had no history of vomiting, convulsions or bleeding from ear, nose and throat. Higher mental functions, all cranial nerves, as well as motor and sensory systems were intact. The neck area was non-tender.

The patient was breathing spontaneously at the rate of 22 breaths per minutes. Oxygen Saturation was 95% on room air. The trachea was central and apex beat at its normal position. On auscultation of the chest, breathing was vesicular, equal in intensity with normal vocal resonance on both sides of chest. Pulse was 88/minutes, regular and moderate in volume. All the peripheral pulses were palpable. Blood Pressure was 99/60 mmHg. Temperature was 37.1 ° C. The abdomen was soft. Tenderness and guarding were absent.

Blood was sent to the laboratory and the results are shown in the tables. CT Scan brain, X-rays cervical spine, chest and both lower limbs were done and these are shown in figures. Ultrasonography of abdomen revealed normal architecture of liver, spleen and kidneys. There was no evidence of free fluid in peritoneal or pelvic cavity.

Figure 1

Table 1: Full Blood Count

Figure 2

Table 2: Coagulation Profile

Figure 3

Table 3: Urine Examination

Figure 4

Table 4:Serum Biochemistry

Figure 5

Table 5: Arterial Blood Gases

Figure 6

Figure 1: X-ray chest AP view (portable). This is an AP & expiratory film so we cannot comment on cardiac shadow. However, there is no evidence of lung contusion, pneumo, haemo or pneumohaemothorax.

Figure 7

Figure 2: X-rays cervical spine lateral projection (Normal)

Figure 8

Figure 3: X-rays left thigh showing mid shaft fracture of femur. The metallic frame used for splinting (immobilization) can be seen.

Figure 9

Figure 4: Fracture right tibia and fibula. Back slab of Plaster of Paris can be seen.

Figure 10

Figures 5: CT Scan brain (plain) showing normal brain.

Figure 11

Management In The Accident And Emergency Unit

Oxygen Therapy:

• O2 inhalation 4/Lwith simple facemask

Fluid Therapy:

• Lactated Ringer's Solution 2000 ml I/V fast

• Then 100 ml/hour

• Blood two units of Packed Red Blood Cells

Analgesia:

• Injection Morphine 5 mg IV prn

• Injection Metoclopramide 10 mg I/V slow stat

• Injection Pethidine 75 mg I/M stat

Antibiotics:

• Injection Ceforoxime 1.5 I/V stat then

• 750 mg I/V 8 hourly

• Injection Metronadazole 500 mg I/V 8 hourly

Prophylaxis against Tetanus:

• Injection Tetanus Toxoid 0.5 ml I/M stat

Wound care

• Dressing of the wounds

• Back slab made of Plaster of Paris was applied on the whole right Lower limb

• Splinting (immobilization) with metallic frame on left lower limb

The patient was kept under keen observations. He could not be transferred to the surgical floor due to unavailability of beds. He was quite stable for about 12 hours. Around 14:00, his heart and respiratory rates then increased gradually and oxygen saturation decreased. However, he was maintaining blood pressure and conscious level. At this point, oxygen therapy was changed to a non-rebreathing face mask. At 17:50 he became drowsy and lost his conscious level completely at 18:00. Heart rate was 140/minute, respiratory rate >35/minute, SpO₂ 78% on FiO₂ 0.8 and BP 110/55 mmHg. He was intubated with pre-oxygenation, Inj. Fentanyl 100µg I/V, Inj. Midazolam 5.0 mg I/V and Inj. Rocurinum 50 mg I/V. Cricoid pressure was maintained with modified Sellick's maneuver. An endotracheal tube sized 8.5 mm ID was passed and fixed at the 20 cm mark at an angle of the mouth after confirmation with an EtCO₂ detector device. Mechanical ventilation was started with a tidal volume of 600 ml and a rate of 12/minute. I: E ratio was kept at 1:2.

Efforts were made to transfer the patient to the Surgical Intensive Care Unit. At 22:00 one bed in the SICU was arranged for this patient. On the way from the Accident and Emergency Department to the SICU another CT Scan of the brain (plain) was done which is shown in figures below.

Figure 12

Figure 6: CT Scan brain (plain) showing poor demarcation between gray and white matter as documented by Neurosurgeon.

Figure 13

Management In The Surgical Intensive Care Unit

At 23:00, the patient was admitted in the SICU sedated, intubated and ventilated. On arrival in the SICU his heart rate was 145/minute, SpO₂ 91% on FiO₂ 1.0, blood pressure 95/60 mmHg. The chest was full of crackles. Ventilation continued with the same ventilatory parameters. Injections of Fentanyl 100µg, Midazolam 2mg and Rocurium 50 mg I/V were given. Sedation and analgesia was started with Propofol 2mg/kg/hour and Fentanyl 50µg/hour infusions respectively. Blood was sent to the laboratory. The results are shown in the tables below.

Figure 14

Table 6: Full Blood Count

Figure 15

Table 7: Serum Biochemistry

Figure 16

Table 8: Coagulation Frofiltable

Different levels of PEEP (0-15cm of water) were also tried. A dobutamine infusion 0-20 mg/kg/minute was started. Senior help was called. Furosemide 100mg and Morphine 20 mg I/V were given. Four units of Red Blood Cells and 500 ml of 5% Albumin were transfused. The central venous line was changed to a pulmonary artery catheter. X-rays of the chest done in the SICU are shown in the following figures.

Figure 17

Figure 7: X-ray chest (AP portable) showing upper lobe diversion and bilateral pulmonary infiltrates.

Figure 18

Figure 8: X-rays (AP portable) showing alveolar pattern pulmonary edema. Pulmonary Artery Catheter was showing Pulmonary Capillary Wedge Pressure of 47 mmHg due to distal kinking of PA catheter. After correction PCWP was found to be 13 mmHg.

The cardiac out put was 8.1 L/minute, cardiac index 3.86 L/minute/m², system vascular resistance 483 dynes.s.cm^-5, pulmonary artery pressure 68/53 mmHg, central venous pressure +7 mmHg, temperature 38.3 °C and pulmonary capillary wedge pressure 13 mm Hg reflecting early sepsis as well. At this point a Nor-adrenaline infusion with 0-20µg/minute was started. The blood pressure dropped to 80/45 mmHg at 01:00 hours. An adrenaline infusion of 0-20µg/minute was also started. He also received some boluses of Metaraminol 0.5-1.0 mg I/V prn. Serial arterial blood gases (ABGs) were done showing progressive acidosis, hypercapnia and severe hypoxemia. Sodium Bicarbonate 8.4% 50 ml was also given. The results of the ABGs are shown in the table below.

Figure 19

Table 9: Arterial Blood Gases

At 03:25 hours, the patient developed bradycardia and hypotension. Five minutes later, cardiac arrest occurred. Code Blue was initiated and full cardiopulmonary resuscitation performed for 30 minutes. He was declared dead at 04:00 hours.

Discussion

In 1861, Zenker₁ described the presence of fat droplets in the lungs of a railway worker who had suffered a severe thoraco-abdominal crush injury at autopsy and later in 1873, Bergmann₂ clinically diagnosed Fat Embolic Syndrome in a patient with fracture of the femur. The work continued on understanding the pathophysiology and pathogenesis of fat embolism throughout the early 20^th century and in 1969, Peltier₃ published his work on the pulmonary consequences of fat rmbolism and its treatment. Gurd₄ in 1970 put together the various clinical manifestations, which he later called the Fat Embolic Syndrome.

The risk of Fat Embolic Syndrome is the greatest in the multiply injured patient, especially those with femoral fractures accompanied by other long bone fractures. Magerl et al₅ in 1966 studied 4,197 fractures and found the incidence of Fat Embolism Syndrome to be 0.9%, where as in a similar study by Peltier et al ₆ in 1974 an incidence of 1-2.2% for tibia and femur fractures was described. Ganong₇ in 1993 found much higher rates of fat embolism. The overall incidence rate of fat embolism was found to be 23% (19 % in tibia versus 75% in femur bone fractures). Collins et al₈ reported that closed fractures had a higher incidence of Fat Embolic Syndrome compared to open fractures. This was thought to be because the intramedullary bone pressure is lower in case of open fractures, which reduces the bulk of fat emboli propelled into the blood stream.

Two events promote entrance of marrow contents into the circulation following a fracture: movement of unstable bone fragments and reaming of the medullary cavity for the placement of an internal fixation device. Fat Embolic Syndrome is also reported after non-traumatic lesions such as DM, severe burns, pancreatitis etc. Age seems to be a factor in the development of Fat Embolic Syndrome; young men with fractures are at increased risk.

There are two theories about the pathogenesis of Fat Embolism, which are widely accepted among the physicians.

• The mechanical theory states that Fat Embolic Syndrome results from physical obstruction of the pulmonary and systemic vasculature with embolized fat. In the pulmonary vasculature, they cause ventilation / perfusion mismatch leading to shunting effect.

• The biochemical theory states that circulating free fatty acids derived from fat droplets are directly toxic to pneumocytes and capillary endothelium in the lungs, causing interstitial hemorrhage, edema and chemical pneumonitis.

The possibility of co-existing Shock, Hypovolemia and Sepsis, all of which reduce liver flow, facilitate the pathogenesis of Fat Embolic Syndrome by exacerbating the toxic effects of free fatty acids cannot be ignored.

A thorough knowledge of the signs and symptoms of the syndrome and a high index of suspicion are needed to make the diagnosis.

An asymptomatic latent period of about 12-48 hours precedes the clinical manifestations. The fulminant form presents as acute cor pulmonale, respiratory failure, and /or embolic phenomena leading to death with in few hours of injury.

The respiratory findings range from nearly asymptomatic hypoxemia to ARDS requiring Ventilatory support. Fat droplets are entrapped in the pulmonary capillary beds causing shunting effect (right to left intrapulmonary shunting of deoxygenated blood). These shunts can be obtained by the use of shunt equation

Q·_s/Q·_t = CćO₂ –CaO₂ / CćO₂ - C v--O₂

where

CćO₂ =Oxygen content of ideal pulmonary-end capillaries. (Derived from Alveolar Gas Equation.

CaO₂ = Arterial O₂ content (obtained from Arterial Blood Gases)

C v--O₂ =mixed venous content of O₂ (obtained from Pulmonary Artery Catheter)

or

Shunt lines as shown in figure 9. Note that there is little benefit in increasing FiO₂ in patients with very large shunts. Oxygen therapy do not play any role if the shunt is >30%.

Figure 20

Figure 9: Iso-shunt curves showing the effect of varying amounts of shunt on PaO2.

Moreover, these substances produce local ischemia and inflammation with concomitant release of inflammatory mediators, platelet aggregation, and vasoactive amines.

A whole series of central nervous system disturbance can occur from Cerebral Fat Embolism. The fat droplets that travel through arteriovenous shunts to the brain produce local ischemia and inflammation. Central nervous system dysfunction initially manifest as agitated delirium but may progress to stupor, seizures, or coma and is usually unresponsive to correction of hypoxia. Retinal hemorrhages with intra–arterial fat globules are visible upon fundoscopic examination. Adams₉ described that these changes can occur within the first 24 hours and consists of “cotton wool” exudates and small streaky hemorrhages along the retinal vessels and in the macula region. Also, diffuse edema and pallor also occur in the macula zone.

Tachycardia is one sign that is invariably present in all patients with Fat Embolic Syndrome. This is due to right ventricular strain and is often resistant to therapy. Rarely, systemic fat emboli can affect the heart leading to mottled myocardial necrosis. This can be detected by some non-specific ECG changes such as ST depression, T wave flattening, Av block and bundle–branch patterns.

A petechial rash that appears on the upper anterior portion of the body including chest, neck, upper arm, axillae, shoulders, oral mucous membrane and conjunctivae is considered to be a pathognomic sign of Fat Embolic Syndrome. Gossling et al₁₀ suggested that they occur in 50-60% of patients. Kaplan ET al₁₁ found that they appear on the second or third day after injury and are secondary symptoms. They results from occlusion of dermal capillaries by fat and increased capillary fragility.

Systemic fever is a common early sign of Fat Embolic Syndrome. It is often mild but may reach up to 39.0 °C. Later the onset of pulmonary infection may lead to an additional temperature increase.

Laboratory Studies

Imaging Studies

Differential Diagnosis

Treatment

Prophylaxis Of Fat Embolic Syndrome

Summary

Our patient was 21 years old with history of long bone fractures closed as well as open fractures obtained in a road traffic accident. Other conditions such as brain and lung pathologies were excluded. When we look at the Gurd ‘s criteria three out of four signs namely hypoxemia, CNS depression and pulmonary edema from major criteria and three out of seven, tachycardia, hyperthermia, fall in haematocrit/platelet count from minor criteria were present. Someone said

“ Diseases do not read the text books” but in our case it seems to be they seem to have done it.

Correspondence to

Dr. ALTAF HUSSAIN MBBS; DA; MCPS; FCPS. Department of Anaesthesiology (41) King Khalid University Hospital Post Box No. 7805 Al-Riyadh 11472 Saudi Arabia E-mail: altafdoa@hotmail.com

Acknowledgments