Cerebral Fat Embolism in ICU - Case presentation and discussion

1. Cerebral Fat Embolism in ICU
Dr.Tarek Sabri Helmi
INTENSIVIST
Fujairah Hospital
UAE
17 October 2016

2. History and Presentation
• 25 –year- old Indian male referred to our hospital from port clinic as
he fall in the sea from a ship leader after hitted by heavy object , he
remained in water for 45 minutes before they succeeded to pull
him.
• On our ER he was drowsy hypothermic , hypotensive and
bradycardia ,no head trauma but there was a wound in Lt side of the
neck ,fracture Lt femur and both legs , patient resuscitated in ER and
reheated then CT trauma done to brain ,chest and abdomen , and x-
rays for long bones.
• CT brain was unremarkable , Ct chest revealed bilateral lung
contusions and aspiration ,X-rays of long bones revealed
comminuted fracture of Lt femur and bilateral fracture of both tibia
.

13. Management
• PATIENT ADMITTED TO ICU on 11/12/15 , he was fully conscious
oriented GCS 15/15 , so continued on non invasive ventilation ,
empirical antibiotics started + ICU care bundle ,conscious sedation
given for skeletal traction and external fixation with adequate
analgesia , then continued on morphine 4 mg every 4 hours prn for
pain , blood transfusion started as HB decreased , patient was stable
for 24 hours .
• On 12/12/15 became febrile , suddenly conscious level deteriorated
with no hypoxemia , GCS 8/15 without lateralization then
developed fits , fits aborted immediately and patient intubated
and ventilated , Fat embolism syndrome suspected versus fat
embolism with patent foramen oval or dissecting carotid vessels .

15. Management cont.
• CT brain , chest ,abdomen and neck with angiography done on
14/12/15 , no dissection , normal brain study .
• Transoesophageal Echocardiography don-- revealed intact atrial
septum.
• Patient managed as FAT EMBOLISM SYNDROME –(supportive
measures + methylprednisolone given 10 mg/kg/8h for 24 h +
albumin )

16. Echocardigraphy (TOE).

19. Radiology Report
• CT scan done.No fresh changes as compared to old CT scan finding .
• CT Angio neck REVEALED --The arteries from the aortic arch to the carotid arteries up to the
cerebral branchs in the brain were traced , no evidence of filling defect of embolisim, nor
dissection.
• Head angio CT: REVEALED No evidence of filling defect or cut off at the cerebral arteries and
circle of willis.
• No evidence of acute infract or bleed .
• CT chest Angio: REVEALED -Bilateral posterior & basal lung contusions, more on the Lt. side.
• -No evidence of filling defect of pulmonary emblisom at the pulmonary arteries.
• -No evidence of hemo pneumothoax .
• CT ABDOMEN (With i.v. contrast on venous ): REVEALED No free fluid or free air in abdomen,No
associated bowel distension ,Normal liver parenchyma and gall-bladder,Normal pancreas,
spleen and kidneys.
• Empty urinary bladder, containing foleys, ballon ,No evidence of bony fracture

20. Complications
Pneumonia MODS

21. Fractures Fixation
• On 20/12/15 as conscious level not improving on interrupting
sedation and MRI was not working so INTERNAL FIXATION don for
all fractures in one setting by ORTHOPEDIC TEAM.

27. MRI REPORT
• MRI and MRA brain don on 21/12/15 , revealed On the T2-
weighted images, and diffusion DWI show multiple nodular or
punctate foci of high signal intensity were found within the brain
parenchyma.
• The lesions were located in the white matter (subcortical white
matter and centrum semiovale) as well as in the gray matter (basal
ganglia and thalami).
• This appearance is highly suggestive of fat embolism syndrome.The
rest of the study is normal and unremarkable , MRA --revealed
intact cerebral vesseles .--

28. Complications cont. (pneumonia with sepsis )
• 22/12/15 assessment of conscious level don , Patient was fully conscious ,
oriented , GCS 14/15 , but with techy cardia du to fever , fever was started on
19/12 , on and off , then become persistent , chest xray revealed pneumonia ,
so antibiotic changed to tazocine and gentamycin empirically .
• On 23/12/15,patient developed recurrent tonic colonic fits, anti-epileptic
started by neurologist (phenytoin)..
• On 24/12/15 fever subsided and patient improved , blood C/S revealed gram
negative bacilli , on 25/12/15 revealed as Acinetobacter sensitive to tegicyclin
only .
• gentamycin stopped and continued on tazocine plus tegecyclin and blood
culture repeated to confirm the results , 2nd blood c/s confirmed Acinetobacter
infection , so colistin added , tazocin stopped after 5 days of treatment .

30. Extubation
• On 26/12/15 Patient was fully conscious , oriented a febrile temp
36.8 , BP 120/68, HR 98 /m regular , SpO2 99% on FiO2 40%, ABG
(pH 7.38 , PaO2 120 , PaCO2 38 , HCO3 20 ), patient EXTUBATED
without complications .

32. Complications (Drug eruption)
• on 27/12/15 Patient is fully conscious , oriented a febrile , Stable
vitals But he developed Skin rash on both shoulder (pustules acne
like ) , discussed with neurologist --plan to withdrawal phenytoin ,
seen also by dermatologist ,diagnosed drug eruption du to
phenytoin .

34. Discharge from ICU
• ON 28/12/15
• Patient was fully conscious , oriented a febrile temp 36.8 , He is on
regular paracetamol 8 hourly PRN for pain , BP 112/64 , HR 94 /m
regular , spo2 99% on fio2 28% through nasal cannula , discussed
with orthopedist and infection control --planning to shift him to
isolated room in the ward ,to continue colistin/tegecyclin to complet
7 days , repeat blood c/s and sputum c/s tomorrow , stop phenytoin
, continue on levitracetam 1gm bid and to be to be followed by
neurologist

35. FAT EMBOLISM SYNDROME(FES)

36. History
• First diagnosed in 1873 by Dr Von Bergmann
• In 1879 Fenger and Salisbury published description of Fat embolism
syndrome

37. Fat Emboli: Fat particles or droplets that
travel through the circulation
Fat Embolism: A process by which fat
emboli passes into the bloodstream and
lodges within a blood vessel.
Fat Embolism Syndrome (FES): serious
manifestation of fat embolism occasionally
causes multi system dysfunction, the lungs are always involved and next is
brain

38. FE vs. FES
• Fat embolization is a well-known complication of skeletal trauma and
surgery involving instrumentation of the femoral medullary canal.
• Fat embolism syndrome (FES) is a physiological response to fat within
the systemic circulation.
• Fat embolization and FES are not synonymus.
• The embolization of fat can be detected in almost all patients who
sustain a pelvic or femoral fracture, but the incidence of FES is less than
1%.

39. Fat Embolism Syndrome
• Mortality: 10-20%
• Clinical diagnosis, No specific laboratory test is diagnostic.
• Mostly associated with long bone and pelvic fractures, and more
frequent in closed fractures.
• Single long bone fracture has 1-3% chance of developing FES, and
increases with number of fractures.
• Onset is 24-72 hours from initial insult.

40. Causes of fat embolism
TRAUMA RELATED:
 Blunt trauma: Long bone (Femur, tibia, pelvic) factures
orthopedic procedures
 Soft tissue injury(chest compression with or without rib fracture)
 Burn
 Liposuction
 Bone marrow harvesting and transplant.

41. NON TRAUMA RELATED
• Pancreatitis
• Diabetes mellitus
• Osteomyelitis and panniculitis
• Bone tumor lysis
• Steroid therapy
• Sickle cell hemoglobinopathy
• Alcoholic liver disease
• Fat infusion

42. • Most common cause of FES is blunt trauma.
• 90 % occurs after blunt trauma complicated by long-bone fractures
• Closed fractures had higher incidence compared to open fractures.
The intramedullary bone pressure is lower in case of open fractures,
which reduces the bulk of fat emboli propelled into the blood stream.

43. Non-traumatic fat embolism
• It occurs due to the process of fat or marrow necrosis or by the
increased concentration of lipids in the blood.
• It may be caused by agglutination of chylomicrons and VLDL by high
levels of plasma CRP.
• As in Acute pancreatitis in patients with types I, IV, and V
hyperlipidaemia and avascular necrosis of bone in patients with
corticosteroid-induced hyperlipidaemia.

44. Pathophysiology of FES
Exact mechanism unknown, but two main hypothesis
1. Mechanical Hypothesis
2. Biochemical Hypothesis

45. • Smaller fat droplets travel through the pulmonary capillaries into the systemic
circulation: Embolization to cerebral vessels or renal vessels also leads to central
nervous system and renal dysfunction

46. Biochemical Hypothesis
Toxicity of free fatty acids
• Circulating free fatty acids directly affect the pneumocytes, producing
abnormalities in gas exchange.
• Coexisting shock, hypovolemia and sepsis impair liver function and
augment toxic effects of free fatty acids.

47. • Hormonal changes caused by trauma or sepsis induce systemic
release of free fatty acids as chylomicrons.
• Acute-phase reactants( C-reactive proteins) cause chylomicrons to
coalesce.
• It explains non traumatic forms of fat embolism syndrome and why
symptoms take 12 hours to develop.

48. FE in ARDS
• Fat emboli obstructs lung vessel
(20microns), platelets and fibrin
adhere to it
• Lipase increases FFA
• Inflammatory changes-
>endothelial damage->ARDS

49. TRAUMA

50. CLINICAL FEATURES
Asymptomatic for the first 12-48 hours
Pulmonary Dysfunction
Neurological (nonspecific)
Dermatological Signs

51. Hypoxemia
Neurological
abnormalities
Petechial
rash

52. Pulmonary
• Hypoxia, rales, pleural friction rub
• ARDS may develop.
• CXR usually normal early on, later may show ‘snowstorm’ pattern-
diffuse bilateral infiltrates
• CT chest: ground glass opacification with interlobular septal
thickening.

53. Neurological findings
• Usually occur after respiratory symptoms
• Incidence- 80% patients with FES
• Minor global dysfunction is most common-ranges from mild delirium to
coma.
• Seizures/focal deficits
• Transient and reversible in most cases.
• CT Head: general edema, usually nonspecific
• MRI brain: Low density on T1, and high intensity T2 signal, correlates to
degree of impairment.

54. Dermatological findings
• Petechie
• Usually on conjunctiva, neck, axilla, upper limbs.
• Results from occlusion of dermal capillaries by fat globules and then
extravasations of RBC.
• Resolves in 5-7 days. Usually fast resolving.
• Pathognomic, but only present in 20-50% of patients.

55. Other findings
• Retinopathy (exudates, cotton wool spots, hemorrhage)
• Lipiduria
• Fever
• DIC
• Myocardial depression (Right heart strain)
• Thrombocytopenia/Anemia
• Hypocalcemia.

56. Diagnostic Criteria
• Gurd criteria most commonly
used.
Other indexes are
• Schonfeld Index
• Lindeque Index

57. Gurd & Wilson Criteria

58. Schonfeld Fat Embolism Syndrome Index
• It ranks signs and symptoms of FES in relation to their incidence of
presentation.
• Score >5 required for diagnosis of fat embolism syndrome

59. Schonfeld FES Index
sign score
Petechial rash 5
Diffuse alveolar infiltrate 4
Hypoxemia pao2<70 mm Hg, FIO2-100% 3
confusion 1
Fever ( >100.4 F) 1
Heart rate >120 beats/min 1
Respiratory rate >30/min 1

60. Lindeque's criteria
• Acc. to Lindeque FES can be diagnosed on the basis of respiratory
system involvement alone.

61. Laboratory Studies
• Arterial Blood Gases (ABGs)
• Urine and sputum examination
• Haemotological Tests
• Biochemical tests

62. Imaging
• Chest x-ray
– shows multiple flocculent shadows (snow storm appearance). picture may be
complicated by infection or pulmonary edema.

63. Imaging contd.
• MRI Brain
- Image showing minimal hypodense changes in
periventricular region, which are more evident in DWI and T2WI as
areas of high signals.

64. Treatment and management
Prophylaxis
• Immobilization and early internal fixation of fracture.
• Fixation within 24 hours has been shown to yield a 5 fold reduction in
the incidence of ARDS.
• Continuous pulse oximeter monitoring in high-risk patients may help
in detecting desaturation early, allowing early institution of oxygen
and possibly steroid therapy.
• High doses of corticosteroids.

65. Supportive Medical Care
• Maintenance of adequate oxygenation and ventilation
• Maintenance of hemodynamic stability.
• Administration of blood products as clinically indicated.
• Hydration
• Prophylaxis of deep venous thrombosis .
• Nutrition.
Treatment and management contd.

66. Treatment and management contd.
Oxygenation and ventilation
• High flow rate oxygen is given to maintain the arterial oxygen tension
in the normal range.
• Mechanical ventilation and PEEP may be required to maintain arterial
oxygenation.

67. Treatment and management contd.
Hemodynamic stability
• Maintenance of intravascular volume is important, because shock can
exacerbate the lung injury caused by FES.
• Albumin has been recommended for volume resuscitation in addition
to balanced electrolyte solution, because it not only restores blood
volume but also binds with the fatty acids and may decrease extent of
lung injury

68. Steroids
• Steroid prophylaxis is controversial to prevent FES.
• It causes blunting of inflammatory response and complement activation
• Prospective studies suggests prophylactic steroids benefit in high risk
patients.
• Preoperative use of methylprednisolone may prevent the occurrence of
FES
• Once FES established, steroids have not shown improved outcomes.

69. Results of Randomized, Controlled Trials of Corticosteroids for Prevention of Fat Embolism Syndrome
Dose Model Timing Duration of study Effect on disease
incidence
30mg/kg Dog Before event 60min None
10mg/kg q8h for 24
hrs
Human trauma At admission No data Declining
7.5mg/kg q6h for
12hrs or placebo
Human Trauma Within 12hrs 2 days Declining

70. Heparin
• Heparin has also been proposed for treatment as it "clears" lipemic
plasma in vivo by causing the release of lipoprotein lipase into the
circulation, but no evidence exists for its use in FES.

71. Prognosis
• The fulminant form presents as acute cor pulmonale, respiratory
failure or embolic phenomena, leading to death within a few hours of
injury.
• Most death contributed to pulmonary dysfunction
• Hard to determine exact mortality rate
• Estimated less than 10%

72. SUMMARY
• The incidence of FES ranges from < 1 to 29% in different studies.
• Actual incidence of FES is not known
• A high index of suspicion is needed to diagnose FES.
• A combination of clinical criteria and MRI brain will enable early and
accurate diagnosis of FES.

73. THANK YOU
Mansoura- EGYPT