Fat Embolism &
Compartment
Syndrome
Group C1
Group Members Student ID
Abdul Hazieq Danial Bin Abdul Mutalib SUKD1601644
Che E Laine SUKD1504760
Fathima Fahda Mohamed Jamiu SUKD1602293
Yehyia Mohamed Fahmi Taha Elkhateeb SUKD1500384
Fat Embolism
● Overview
● Pathophysiology
● Clinical Presentation
● Diagnosis
● Management
Fat Embolism Syndrome (FES)
● Is an ill-defined clinical entity that arises from the systemic manifestations
of fat emboli within the microcirculation
● Embolized fat within capillary beds cause direct tissue damage as well as
induce a systemic inflammatory response resulting in pulmonary,
cutaneous, neurological, cardiac, and retinal symptoms
● FES is most often associated with orthopedic trauma. However, rare cases
of FES have been reported to occur following bone marrow
transplantation, osteomyelitis, pancreatitis, alcoholic fatty liver, and even
liposuction
Pathophysiology
● Fat embolism syndrome is a disease affecting mainly capillaries and mainly on the venous
side
● Hence, the lung is the most common organ affected in FES
● However, the fat globules and chylomicrons gain access to the systemic circulation and
can also affect heart, brain, skin, and retina
● The various explanations offered for the systemic manifestations of FES are:
○ Pulmonary A-V malformations
○ Passing of deformed fat globules through pulmonary capillaries
○ Bypassing pulmonary circulation via a patent foramen ovale
○ Re-opening of a closed foramen ovale due to an acute rise in pulmonary pressure
● The symptoms usually occur within 12 h to 72 h, but can occur over a wide range of time
of 6 h to 10 days
Pathophysiology
● Fat particles larger than 10 μm in diameter enter the circulation and cause damage to capillary beds
Formation of fat
embolism
Mechanical theory Biochemical theory
Elevation in intramedullary pressure Inflammatory response to trauma
Release of fat through open venous Release of free fatty acids from the
sinusoids bone marrow into the venous system
Elevated free fatty acids as well as
Embolized fat obstructs capillary
the inflammatory mediators cause
beds
damage to capillary beds
Free fatty acids have also been shown
Increased capillary bed permeability, damaged to induce inflammation within the
surrounding tissue from inflammatory mediators, and lungs
lung injury that is indistinguishable from ARDS
Clinical Presentation
● FES is a multiorgan disease and can damage any microcirculatory system within the body
● Presenting signs are nonspecific and include tachypnea, tachycardia, and fever
● Pathognomonic signs are petechiae on the trunk and axillae and in the conjunctival folds
and retinae
● The pulmonary circulation is most commonly affected in FES, with up to 75% of patients
experiencing respiratory depression, which can range from mild hypoxia requiring
supplemental oxygen to ARDS requiring prolonged mechanical ventilation
● Patients may decompensate rapidly to respiratory failure
● FES can cause nonspecific neurological symptoms, which are believed to arise from
cerebral edema rather than ischemia, so the symptoms are nonlateralizing
● This includes lethargy, restlessness, or a change in the Glasgow Coma Scale (may become
comatose)
● Microvascular injury of the retina results in hemorrhagic lesion of the retina
● Patients may also develop thrombocytopenia or a decrease in hemoglobin in FES
Diagnosis
Gurd and Wilson's criteria:
Diagnosis
Schonfeld's scoring system:
Lindeque's criteria:
Management
● Once a patient develops FES the only proven treatment is supportive care of the involved
organ systems – manage in the HDU or ICU
● Symptoms of the syndrome can be reduced with the use of supplemental high inspired
oxygen concentrations immediately after injury
● If ARDS develops the patient may require mechanical ventilation while recovering from
lung injury
● The incidence of FES appears to be reduced by the prompt stabilization of long-bone
fractures
● Apley: Intramedullary nailing is not thought to increase the risk of developing the
syndrome
● Schult M, et al.: 12–26% of patients undergoing reamed intramedullary nailing in the
area of the femur develop pulmonary complications
Compartment Syndrome
● Overview
● Pathophysiology
● Clinical Features
● Diagnosis
● Treatment
Compartment Syndrome
● Acute compartment syndrome is a painful condition caused by the
increased interstitial pressure (intracompartmental pressure – ICP) within
a closed osteofascial compartment which impairs local circulation
● Usually the leg and forearm are the most frequently affected, but it can
also involves the hand, thigh, foot, and buttock
● It usually develops after a severe injury such as fractures or crush injury,
but it can also occurs after a relatively minor injury and it may be
iatrogenic
Pathophysiology Bleeding, oedema or inflammation
(infection) may increase the
Necrosis of nerve pressure within one of the
and muscle within osseofascial compartments
the compartment
6 hours or less
Greater increase in Reduction in the
pressure with more capillary flow
profound ischaemia
Muscle ischaemia
with further edema
Pathophysiology
● Nerve is capable of regeneration but muscle,
once infarcted, can never recover and is
replaced by inelastic fibrous tissue
(Volkmann’s ischaemic contracture)
● A similar cascade of events may be caused by
swelling of a limb inside a tight plaster cast
● High-risk injuries are fractures of the elbow,
forearm bones, proximal third of the tibia, and
also multiple fractures of the hand or foot,
crush injuries and circumferential burns.
Clinical Features
Five Ps of ischaemia:
1. Pain (Severe/ “bursting” sensation)
2. Paraesthesia
3. Pallor
4. Paralysis
5. Pulselessness (ischaemia occurs at the capillary level, so pulses may still
be felt and the skin may not be pale)
Diagnosis
● The diagnosis is made on the basis of physical examination and repeated ICP measures
● Physical examination: hyperextension of the toes or fingers causes increased pain in the calf or
forearm (because ischaemic muscle is highly sensitive to stretch)
● Measuring ICP:
○ A manometer is introduced into the compartment and the pressure is measured close to the
level of the fracture.
○ A differential pressure (ΔP) – the difference between diastolic pressure and compartment
pressure – of less than 30 mmHg (4.00 kilopascals) is an indication for immediate
compartment decompression.
Treatment
● The threatened compartment (or compartments) must be promptly decompressed
● Casts, bandages and dressings must be completely removed (merely splitting the
plaster is utterly useless)
● Elevating the limb causes a further decrease in end capillary pressure and aggravates
the muscle ischaemia
● If the differential pressure falls below 30 mmHg or if the surgeon believes there is a
compartment syndrome present regardless of the differential pressure, an
immediate open fasciotomy must performed
Anatomical Compartments Surgical approach
region
Forearm Three: volar, dorsal, lateral. Volar incision.
The volar compartment is the most Dorsal incisions
frequently involved
Hand Ten: Hypothenar, Thenar, Adductor Two longitudinal incisions over 2nd and 4th
pollicis, N.4 dorsal interosseus, N.3 metacarpals.
palmar interosseus Longitudinal incision radial side of 1st metacarpal.
Longitudinal incision over ulnar side of 5th metacarpal.
Carpal tunnel decompression.
Thigh Two: anterior and posterior Single lateral incision
Leg Four: Anterior, Lateral, Posterior Two incisions, medial and lateral, of a minimum of 15
(superficial and deep) cm.
Some surgeons propose a singular lateral approach
Foot Nine: Medial (abductor hallucis and Two dorsal incision, dorsomedial and dorsolateral.
flexor hallucis brevis), Lateral A single medial incision is used by some authors to
(abductor digiti minimi and flexor release all nine compartments
digiti minimi brevis), N. 4 interosseus,
N. 3 central (superficial, central and
deep)
References
1. Apley & Solomon’s System of Orthopaedics and Trauma (2018)
2. Kwiatt ME, Seamon MJ. Fat embolism syndrome. Int J Crit Illn Inj Sci. 2013;3(1):64–68. doi:10.4103/2229-
5151.109426 retrieved from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3665122/#ref13
3. Schult, M., Frerichmann, U., Schiedel, F. et al. Eur J Trauma (2003) 29: 68.
https://doi.org/10.1007/s00068-003-1247-y retrieved from:
https://link.springer.com/article/10.1007/s00068-003-1247-y#citeas
4. George J, George R, Dixit R, Gupta RC, Gupta N. Fat embolism syndrome [published correction appears in
Lung India. 2017 Jan-Feb;34(1):114]. Lung India. 2013;30(1):47–53. doi:10.4103/0970-2113.106133 retrieved
from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3644833/
5. Via AG, Oliva F, Spoliti M, Maffulli N. Acute compartment syndrome. Muscles Ligaments Tendons J.
2015;5(1):18–22. Published 2015 Mar 27. Retrieved from:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4396671/
