Case Study: Typical Bilateral Femoral Fracture: Camarines Sur Polytechnic Colleges

Republic of the Philippines
CAMARINES SUR POLYTECHNIC COLLEGES

Nabua, Camarines Sur
Case Study: Typical Bilateral Femoral Fracture

Abstract
Osteoporosis is a common disease in the elderly, correlated with increased fracture risk,
disability and mortality. Bisphosphonates are efficient and have been widely used in the
treatment of osteoporosis. Nevertheless, long term bisphosphonate use has been linked
with atypical femur fractures. These have a characteristic pattern and history. They
usually occur in the proximal third of the femur, and may be complete or incomplete,
manifesting either like a radiolucent line or just thickening of the lateral cortex. Their
morphology is simple, transverse or short oblique. They are related to minimal, or no
trauma at all, but symptoms do pre-exist long before the gross fracture actually takes
place.
In this paper we report the case of a 75-year-old woman who sustained an atypical right
femur fracture while walking. Her past medical history of osteoporosis treated with
alendronate for six years along with symptoms in the contra-lateral thigh for the past 2
years, lead to imaging of the left femur. Thus, our patient had a complete fracture on the
right side and an incomplete one, represented by lateral cortex thickening on the left.
Treatment consisted of discontinuation of bisphosphonates, intra-medullary nailing of
the right femur and conservative treatment of the left side. Uneventful union occurred on
both sides.
Key words
 Bisphosphonates
 atypical femoral fracture
 osteoporosis treatment
Introduction
Osteoporosis is a common disease in the elderly, associated with a great fracture risk.
That can lead to disability, poor quality of life and mortality. Therapy with most
bisphosphonates has shown to reduce the risk of vertebral, non-vertebral and hip
fractures in women with postmenopausal osteoporosis and are often considered to be
the first choice of treatment [1-4]. Their effectiveness is indicated by reports that
demonstrate up to 50% reduction of vertebral fracture risk and 20-50% of femoral neck
fracture risk [5,6]. Bisphosphonates are also indicated in osteoporotic men with great
fracture risk. However, many cases of atypical femoral fractures have been described
after long-term use of bisphosphonates [7-12]. Dell et al. in 2012, suggested that the
risk for atypical femoral fractures is 1,78/100.000 person-years in patients receiving

bisphosphonates for 6-8 years [13]. On the other hand, other studies suggest that there
is no increase in atypical fractures in bisphosphonate users [13,14]. According to the
ASBMR Task Force paper in 2010, the most common location of the atypical femoral
fractures is the proximal one-third of the femoral shaft, but they can also occur
anywhere along the diaphysis of the femur from just distal to the lesser trochanter to just
proximal to the supracondylar flare of the distal femoral diaphysis [15]. They are
noncomminuted complete fractures with transverse or short oblique orientation or
incomplete manifested with a radiolucent line within the lateral cortex and are related
with low energy trauma or no trauma at all. Most patients often describe a pain in the
groin or thigh several weeks or even months before the fracture. Radiologically, they are
often associated with localized periosteal stress reaction of the lateral cortex and
generalized thickening of the femoral cortex. Many published case reports of
bisphosphonate-related atypical fractures of the femur present unilateral fractures or
bilateral fractures that occurred at different times or both perfect and imperfect
contralateral fracture simultaneously, as described in our case. The treatment is surgical
with intramedullary nailing and at the same time suspension of the bisphosphonate
therapy. Fractures of the femoral head or peritrochanteric region fractures with spiral
extension to subtrochanteric region, pathological fractures related to primary or
metastatic cancer and periprosthetic fractures must be excluded from this category of
atypical fractures [16].
Case report
A 75-year-old patient was transferred with an ambulance to our hospital because of

sharp pain in her right thigh during gait. Clinical examination revealed tenderness,
swelling and paradoxical movement in the middle of the right femur. The radiological
examination showed a fracture of the right femoral shaft.
Patient’s medical history comprises hypertension, carotid stenosis, dyslipidemia,

appendectomy, cholecystectomy and hysterectomy. The patient undergoes therapy with
alendronate for six years due to osteoporosis. The patient also reports occasional
feeling of heaviness in the left thigh over the past 2 years. This information from her
medical history combined with the typical morphology of the fracture (no comminuted
transverse fracture of the femoral shaft), led the diagnostic approach to radiological
investigation of the left femur too. The radiological examination revealed incomplete
atypical fracture of the left femoral shaft with increased thickness of the lateral cortex
(Figure 1).
Figure 1.
AP radiographs of both
femurs. The radiograph of
the right femoral shaft
shows a complete atypical
femoral fracture. The
radiograph of the left
femoral shaft shows an
incomplete atypical
femoral fracture with
increased thickness of the
lateral cortex associated
with a radiolucent
horizontal line
Blood tests results: Ca=9.2mg/dl(8.4-10.2), P=3.9mg/dl(2.5-5.0), ALP=44U/L(40-150),

25(OH)D3=22.30ng/ml(30-100), iPTH=69.02pg/m (15-80), NTx=12.1(6.2-19),
PINP=42.4ng/ml(16.3-73.9) and Ca markers (CEA, CA15-3, CA-125, AFP, CA19-9) are
within normal values. The bone density scan that was performed during the days of
hospitalization, using DEXA method in the lumbar region and in the left hip, revealed
osteopenia. The DEXA showed L2-L4 BMD of 0.761 g/cm2 – T-score: -2.02 SD, neck of
the left hip BMD of 0.702 g/cm2 – T-score: -1.9 SD and total hip BMD of 0.779 g/cm2 –
T-score: -1.9 SD. Laboratory results of the patient performed previously presented
normal values of ALP, thus excluding hypophosphatasia from differential diagnosis.
According to the newest guidelines of the ASBMR (American Society of Bone and
Mineral Research), the patient underwent intramedullary nailing of the right femur and
was instructed to discontinue bisphosphonate along with non-weight bearing of the left
lower extremity [17-19]. Although a bone scan was conducted for further investigation of
the incomplete fracture and the presence of other imperfect fracture sites, no new
lesions were found (Figures 2&3). After 6 weeks, there was a clinical improvement in
the left femur and radiographic appearance of callus, thus excluding the prophylactic
intramedullary nailing of the left femur. The union of both fractures developed normally
both for the right femur which was treated with intramedullary nailing and the left femur
where conservative treatment was selected. The union of the right femur was not
affected by the fact that the distal locking screw was not centered in the nail hole. The
radiographic monitoring of the bone healing was conducted at 3, 6 and 12 months after
the first treatment took place (Figures 4&5).
Figure 2. Bone scan
Figure 3. Bone scan

Figure 4. Postoperative radiographs taken two and six months after surgery. The left
one shows one AP view of the femoral shaft with the IM nail. The other two shows one
AP and P view of the upper one half of the femur
Figure 5. AP radiograph of both femoral shafts 1-year after surgery
Discussion
The administration of bisphosphonates for the therapy of osteoporosis is effective and
well tolerated, but long-term administration has been associated with fractures of the
femoral shaft and subtrochanteric area. In addition, there is great interest concerning
the incidence, etiology and pathophysiology of this kind of fractures. According to the
ASBMR Task force, atypical femoral fractures are stress fractures that are unable to
heal secondary to the suppression of remodeling due to the bisphosphonate treatment.
Also, the primary location in the lateral cortex suggests that reduced tensile strength
may be another possible pathogenetic mechanism, propably due to the changes in
bone properties as a result of low bone turnover. There are also several other
mechanisms proposed for the pathophysiology and etiology of atypical femoral
fractures, but their correlation with long-term use of bisphosphonates still remains
unclear [17]. Reviewing international literature, many cases of atypical femoral fractures
have been referred, demonstrating the hazards of long term administration and the
necessity for close supervision of this group of patients to detect early symptoms [20-
22]. Studies on effectiveness of antiosteoporotic drugs have measured hip fractures in
general and not femoral neck fractures or intertrochanteric in particular. A systematic
review and meta-analyses of 5 case control studies and 6 cohort studies has suggested
that there is a RR=1.70 of subtrochanteric, femoral shaft and atypical fractures of the
femur amongst bisphosphonate-treated patients and RR=11.78 when studying in
particular atypical femoral fractures and bisphosphonate exposure [23]. However, there
is still no consensus regarding the pathogenic mechanism that is responsible for
causing atypical fractures after the long-term use of bisphosphonates, as suppression of
bone remodeling that was previously described is common to all patients taking
bisphosphonates and not only to those who suffered the atypical fracture.
The optimal duration of bisphosphonates use is not clear. Because of their high affinity
to hydroxyapatite, they remain on bone surfaces for a long period. That is why when
osteopenia levels are achieved, their administration should be discontinued for 3-5
years and then resumed again if needed [24]. Teriparatide, a recombinant form of
parathyroid hormone(PTH), has shown benefits on treatment of atypical femoral
fractures [25-27]. It acts as an anabolic agent by inducing the formation of new bone
and by reversing the suppression of bone turnover that is caused by bisphosphonates,
which might be a possible mechanism of atypical femoral fractures. The limited data
available for the beneficial effect of Teriparatide on fracture healing leads to the
necessity for further investigation relative to its use in the treatment of atypical femoral
fractures.
Most of the atypical femoral fractures, according to the literature, that are associated
with administration of bisphosphonates such as alendronate, differ from common
osteoporotic fractures, high-energy fractures and periprosthetic fractures and include:
low-energy trauma or no trauma, history of alendronate use for osteoporosis after
menopause, onset of spontaneous thigh pain before the fracture, different location than
common osteoporotic fractures (spine, hip, wrist), bilateral presentation (sequentially or
simultaneously), hypertrophy or increased thickness of the cortex at the radiographs in

the fracture site, an uncommon form of fracture (transverse or short oblique) and
delayed healing time [28].
Several cases of patients that sustained atypical femoral fractures after long-term
administration of bisphosphonatesare reported in international literature [29,30]. The
majority of fractures occurred after oral administration of alendronate (> 95%) and the
rest after oral administration of risedronate and intravenous administration of
pamidronate and zoledronate. In few of these case reports, there was reference in bone
turnover markers and in even fewer of them these markers were reduced [24]. In a
recent prospective study of 100 asymptomatic patients receiving bisphosphonates for
over 3 years, the incidence of incomplete atypical femoral fractures was 2% [31]. The
majority refers to unilateral fractures or sequential bilateral fractures which are reported
up to 28% of the patients, or perfect and imperfect simultaneous contralateral fracture,
as happened in our case [31]. There are very few reports for simultaneous perfect
bilateral atypical femoral fractures or simultaneous bilateral femoral fractures without
prior use of drugs that affect bone metabolism.
The occurrence of atypical fractures after long-term administration of bisphosphonates,
strongly differs among patients and possibly the administration of drugs which alter the
bone turnover rate can affect some patients more than others. If this point of view is
correct, then this characteristic side effect of bisphosphonates and other anti-
osteoclastic drugs is probably due to genetic differences and not due to anti-osteoclastic
drugs [32]. The future solution will be to identify the corresponding genes and take
precautions when administering this kind of drugs to people who have those genes [33].
In the case report that we present, the treatment was selected according to the newest
guidelines of ASBMR Task Force and involved surgical treatment for the complete
fracture and conservative treatment for the incomplete fracture while suspending the
administration of bisphosphonates, which is mandatory.
Conclusion
The rational use of bisphosphonates is crucial to minimize the risk of osteoporotic
fractures and atypical femoral fractures. The presentation of this incident demonstrates
the importance of close observation of those patients who undergo bisphosphonate
treatment, so that we can recognize prodromal symptoms of atypical fractures of the
femur and avoid such complications, and the need for personalized treatment according
to guidelines in patients with atypical femoral fractures.
Competing interests
No relevant disclosures
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Case Study: Haemorrhagic shock following

massive subcutaneous haematomas of the lower
back due to blunt trauma
Abstract
An 83-year-old woman with no significant medical history was transferred to our tertiary
hospital after being hit by a car and presenting with haemorrhagic shock. Immediate
fluid resuscitation was performed; physical, chest/pelvic X-ray and echographic
examinations did not detect any major sources of bleeding. However, a contrast-
enhanced CT scan revealed multiple regions of significant contrast extravasation in an
extensive part of the subcutaneous tissue of the patient's lower back, which is an
unusual source of bleeding. Transcatheter arterial embolisation of the lumbar and
internal iliac arteries and their branches was carried out. In addition, haemostatic
resuscitation was performed for damage control resuscitation, which successfully
resolved the patient's haemorrhagic shock.
Background
Lumbar artery injuries, which are not a major source of internal bleeding, can cause
significant retroperitoneal haemorrhaging and are associated with a high mortality
rate.1 2 As chest/pelvic X-ray and echographic examinations, and focused assessment
with sonography for trauma (FAST) cannot exclude certain types of internal bleeding,
such as retroperitoneal or non-cavitary haemorrhaging, 3 clinicians should take such
injuries into consideration in patients with haemorrhagic shock of unknown origin. We
describe a case in which massive subcutaneous haematomas of the lower back, which
are an unusual source of bleeding, occurred after blunt trauma, and were successfully
treated with haemostatic resuscitation, and transcatheter arterial embolisation of the
lumbar and internal iliac arteries and their branches.
Case presentation
An 83-year-old woman with no significant medical history was transferred to our tertiary
hospital after being hit by a car while walking on the road. On arrival, she was pale and
significantly distressed, and exhibited the following signs of shock: Glasgow Coma
Scale 12 (E4V3M5), respiratory rate 25 breaths/min, heart rate 99 bpm and blood
pressure 42/28 mm Hg. Fluid resuscitation was started immediately and tracheal
intubation was performed due to suspected severe haemorrhagic shock.
Simultaneously, a massive transfusion protocol was initiated, which enabled the infusion
of red blood cells and fresh frozen plasma 30 min after the patient’s arrival. A physical
examination did not reveal any obvious head, neck, chest, abdomen or pelvic traumas
other than an obvious deformity of her right lower extremity associated with an open
wound. Six hours after her arrival, following her recovery from haemorrhagic shock, the
patient's posterior region was assessed, which resulted in the detection of multiple
subcutaneous haematomas covering an extensive region of her lower back (figure 1).
Chest X-ray and ultrasound examinations excluded a cavitary haemorrhage and
intrathoracic, intra-abdominal or pericardial effusion, and a pelvic X-ray showed that the
patient’s fractures were stable. As the patient exhibited a transient response to fluid
resuscitation, she had been moved to the CT suite 40 min after her arrival to identify any
major sources of bleeding. A contrast-enhanced whole-body CT scan detected multiple
regions of subcutaneous contrast extravasation in her lower back (figure 2A, B). In
addition, a Chance fracture of the first lumbar vertebra, a left-sided psoas haematoma
associated with multiple fractures of the transverse processes of her lumbar vertebrae
(figure 3A, B), and open fractures of her left lower extremities, were also identified. The
pelvic fractures proved to be those of pubic and ischium bone on the left side, and third
and fourth sacral bone fractures with stable pelvic ring, which were rated as 61-A by
Orthopaedic Trauma Association classification (figure 4). Large retroperitoneal
haematoma associated with pelvic fracture was absent on initial CT scan. The
subcutaneous soft tissue of the patient’s lower back was determined to be the major
source of her bleeding, and concomitant retroperitoneal haemorrhaging associated with
the fractures of the transverse processes of her lumbar vertebrae was also considered
to have contributed to her bleeding.
Figure 1
An image of the patient’s
posterior region taken 6 h
after arrival. The patient’s
shock had been resolved by
the time this image was
taken. Significant
subcutaneous haematomas
were noted in the lower back (triangle arrow) together with bruising in the iliac crest
area.
Figure 2
A contrast-enhanced CT scan revealing multiple regions of contrast extravasation in the

subcutaneous tissue of the patient’s lower back ((A) early phase and (B) delayed
phase).
Figure 3
Retroperitoneal haematoma associated with fractures of the transverse processes of

the lumbar, which was not significant (yellow arrow). Multiple contrast extravasations
and haematoma were seen in the subcutaneous region of lower lumbar level (yellow
triangle arrow) ((A) at the level of the 2nd lumbar and (B) at the level of the 4th lumbar).
Figure 4
Stable-type pelvic fracture, which was classified as 61-A by Orthopaedic Trauma
Association classification.
Investigations
The initial arterial blood gas analysis revealed an elevated serum lactate concentration
together with the following findings: pH 7.380, PaCO 2 38.3 mm Hg, PaO2 501.1 mm Hg,
haemoglobin level 10.2 g/L, base excess −2.1 mmol/L and lactate 4.1 mmol/L on 10
L/min of oxygen directly prior to intubation.
The patient’s laboratory data on arrival were indicative of acute traumatic coagulopathy:
platelet count 13.8×104/μL, international normalised ratio 1.22, fibrinogen 98 mg/dL and
D-dimer 100.8 μg/mL.
Treatment
The patient was taken to the angiography suite soon after undergoing a CT scan so that
the bleeding could be stopped. Aortography detected active contrast extravasation at
multiple sites located close to the bilateral lumbar and internal iliac arteries (figure 5).
The affected vessels included the first, second and fourth lumbar arteries on the right
side, and the bilateral third lumbar artery and the bilateral superior gluteal arteries (left
side dominant). Ultimately, to complete the haemostatic procedure, the embolisation of
these affected lumbar arteries and the bilateral internal iliac arteries was successfully
performed using an absorbable gelatine sponge. The patient required 18 units of red
blood cell concentrate, 20 units of fresh frozen plasma and 20 units of platelets within
12 h of her arrival for haemostatic resuscitation, which successfully resolved her
haemorrhagic shock. On the third day, a posterior spinal fusion procedure was
performed for the Chance fracture of the first lumbar vertebra. The patient was
successfully extubated on the 16th day. On the 23rd day, the open fracture of her right
lower extremities was subjected to internal fixation.
Figure 5
An aortographic image showing multiple
regions of contrast extravasation. The
lumbar and internal iliac arteries and their
branches were located in the affected
region (white triangle arrows describe the
bilateral lower lumbar arteries, and yellow
ones describe the superior gluteal artery on
the left side).
Outcome and follow-up

The patient was transferred to another hospital on the 31st hospital day. At 90 days after
suffering the injury, the patient was undergoing rehabilitation.
Discussion
Exsanguination is a leading cause of death in trauma patients. Internal bleeding after
blunt trauma most commonly occurs in the intra-thoracic, intra-abdominal and
retroperitoneal spaces (bleeding in the retroperitoneal space is often associated with
pelvic fractures).Although chest/pelvic X-ray and focused assessment with sonography
for trauma (FAST) examinations can identify such internal bleeding, other types of
internal bleeding, for example, retroperitoneal haemorrhaging from other sources or
non-cavitary haemorrhaging, cannot be detected by these techniques.Pedowitz and
Shackford reported that about half of trauma patients who present with shock are
subsequently found to be suffering from non-cavitary haemorrhaging, which is
associated with long bone fractures or skin lacerations. Therefore, clinicians should
recognise that less common types of internal bleeding, such as non-cavitary
haemorrhaging, can also cause significant bleeding.
While pelvic fractures are a major cause of massive retroperitoneal
haematomas, lumbar artery injuries are a rare source of post-blunt trauma
bleeding.Lumbar artery injuries are commonly associated with transverse process
fractures of the lumbar vertebrae. Our patient had stable pelvic fractures and
retroperitoneal haematomas associated with transverse process fractures of the lumbar
vertebrae, which are not commonly associated with major bleeding. However, she
developed massive subcutaneous haematomas covering an extensive region of her
lower back, which was served by the bilateral lumbar and internal iliac arteries and their
branches. These kinds of injuries are difficult to identify during physical, pelvic X-ray or
echographic examinations. Thus, contrast-enhanced CT scans are essential for
detecting the source of bleeding in such cases. The mechanism responsible for these
types of injuries is considered to involve sclerotic changes making the arteries
vulnerable to injury during high-energy impacts, resulting in significant subcutaneous
haematomas developing in elderly patients.
As for treatment, transcatheter arterial embolisation of the affected vessels is effective

at controlling retroperitoneal and subcutaneous haemorrhaging. Open surgery is not
recommended because it often fails to identify the source of the bleeding and can cause
further bleeding due to decompression.7 In addition to controlling any haemorrhaging,
haemostatic resuscitation based on the concept of damage control resuscitation is also
crucial to resolving acute traumatic coagulopathy.
We described a case in which massive subcutaneous haematomas developed in an
extensive region of the lower back. The haematomas were associated with injuries to
the lumbar and internal iliac arteries and their branches, which are unusual sources of
bleeding after blunt trauma. The ‘historical’ or ‘traditional’ initial screening of a bleeding
trauma patient (chest X-ray, pelvic X-ray and FAST) has many limitations and can often
fail to determine the origin of unexteriorised bleeding. In our case, a contrast-enhanced
CT scan identified the source of bleeding, and the patient was successfully treated with
transcatheter arterial embolisation and haemostatic resuscitation.
Learning points
 Subcutaneous haemorrhaging in an extensive area of the lower back associated
with injuries to the lumbar and internal iliac arteries and their branches can cause
major bleeding in elderly patients who suffer blunt traumas.
 As the ‘historical’ or ‘traditional’ initial screening of chest/pelvic X-ray and FAST
cannot detect such injuries, for example, non-cavitary haemorrhaging, contrast-
enhanced CT scans are necessary for identifying the source of bleeding.
 Transcatheter arterial embolisation and haemostatic resuscitation are effective at
resolving shock.
References
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Case Study: Methanol Poisoning in a Child

Abstract
A girl admitted to the emergency room with a history of four hours' acute illness,
characterized by nausea, vomiting, salivation, headache, blurred vision, and acidotic
“Kussmaul” breathing. Arterial blood gases showed severe mixed acidosis, metabolic
and respiratory with high anion gap. She had ingested the contents of a scent bottle
containing methanol, which she thought was a soft drink bottle. The girl was managed
with hemodialysis and strong intravenous hydration. She improved well and made a full
recovery.
Introduction
Methanol poisoning in children is rarely described in the literature; some cases are
reported as accidental ingestion. For this reason, we report here a case of accidental
methanol poisoning, discussing clinical and laboratory manifestations, management,
and evolution.
Case Report
A six-year-old female patient was admitted to the emergency room with her mother after
four hours of disease characterized by nausea and vomiting of food content, abdominal
pain, difficulty in breathing, salivation, headache, blurred vision, and psychomotor
agitation. A physical examination found the following: weight 22 kg, blood pressure
80/60 mmHg, respiratory rate 32 breaths per minute, and heart rate 148 beats per
minute.
Her skin was pale, and her eyes were sunken, underactive, clouded, and irritable to
stimulus.
The patient was initially treated for severe dehydration resulting from food poisoning.
However, with the development of wheezing and unresponsiveness to stimuli, she was
transferred to the shock trauma unit for worsening respiratory distress, deep breathing
with panting (Kussmaul) breathing, unresponsiveness to stimuli, Glasgow 10, to receive
ventilator support.
The laboratory findings were as follows: yellow urine, specific gravity 1.025, pH 7.0,
trace glucose, leukocytes 8−10x field, erythrocytes 2-3x field, the leukocyte blood count
8,180x mm3, segmented 69%, eosinophils 5%, lymphocytes 26%, Hb 12 g/dL, sodium
133 mEq/L, potassium 6 mEq/L, chloride 107 mEq/L, aspartate aminotransferase 4490
IU/L, alanine aminotransferase 8030 IU/L, and lactate dehydrogenase 2609 UI/L.
Arterial blood gases showed severe mixed acidosis, metabolic and respiratory with high
anion gap (pH 6.9, PaO2: 108 mmHg, PaCO2: 26 mmHg, and HCO3: 3 mEq/L). We
therefore assumed the possibility of diabetic ketoacidosis, salicylate poisoning, or
methanol poisoning. Evaluation of renal function showed urea 33 mg/dL and creatinine
0.6 mg/dL; glucose was normal. Therapy was initiated with vigorous hydration with
sodium chloride 9/1000 and supplemental intravenous sodium bicarbonate. The
toxicology results showed a serum methanol of 1.47 mg/dL. Emergency hemodialysis
therapy was initiated; the patient was dialyzed for an hour for two sessions.
The family gave us new information that the girl regularly took a drink called Kola Ingles.
They stated that the patient had found a 250 mL pink perfume bottle and that she had
ingested 200 mL of its contents, thinking it was the cola drink.
The patient improved progressively after hemodialysis with correction of her metabolic
acidosis, liver function tests, and lactic dehydrogenase (Tables 1 and 2).
The child was discharged from the hospital in five days recovering full health.
Discussion
Methanol (CH3OH), also known as methyl alcohol, wood burning alcohol, or carbinol, is
highly toxic. It is the simplest of the alcohols used in paints, varnishes, solvents,
perfumes, plastic manufacture, photographic materials, antifreeze, and household
cleaning products.
The pathways for poisoning are inhalation, cutaneous, and digestive tract, in most
cases by swallowing. Methanol poisoning in children is rare and there are only isolated
reports of homicidal poisoning and seizures.
In some European countries, it is reported that the main cause of hospitalization among
teens is alcohol poisoning. Reasons range from recreational use to poisoning and self-
harm.
Sometimes symptoms may mask an underlying condition, which may delay diagnosis.
Individual or collective poisoning is usually voluntary or accidental ingestion in the case
of adulterated liquor.
The stages of intoxication are described as follows. In the first phase, there is minimal
decrease in central nervous system activity, weakness, dizziness, and nausea. The
second phase is marked by the development of metabolic acidosis characterized by
vomiting, abdominal pain, confusion, visual disturbances, photophobia, blurred vision,
bilateral mydriasis, unresponsiveness to light, and occasional blindness. In the third
phase, in direct relation to the degree of metabolic acidosis, neuronal injury occurs with
retinal necrosis and hemorrhage in the basal ganglia of the brain. At this stage there is
hypotension, coma, and Kussmaul breathing. Our patient was considered to be in the
second phase of methanol toxicity.
Diagnosis of methanol poisoning is based on the suspicion of ingestion, the presence of

visual disturbances, the onset of metabolic acidosis with elevated anion and osmolar
gaps, and markedly increased liver enzymes.
Confirmation is by determining the plasma levels of methanol. The toxic methanol dose
is 10–30 mL (100 mg/kg), although lower intakes have caused blindness. It is lethal
above 60–240 mL (340 mg/kg). A dose of 30 mL of 100% methanol can be considered
fatal.
Concentrations above 0.2 g/L are toxic, values higher than 0.5 g/L indicate severe
poisoning, and concentrations above 0.9 g/L are potentially deadly.
Methanol is rapidly absorbed from the gastrointestinal tract, giving peak plasma levels
after 30–90 minutes. The serum half-life ranges from 14 to 30 hours and is distributed
freely. The kidney, in untreated patients, removes less than 5%.
In the liver, methanol is removed by biotransformation via alcohol dehydrogenase

(ADH), forming formaldehyde, and subsequently through conversion of the aldehyde
dehydrogenase to formic acid.
That methanol by itself is not toxic. It is the degradation of methanol by alcohol

dehydrogenase that releases the toxic metabolites, formaldehyde, and formic acid.
The rational for treatment is reducing the formation of the toxic metabolites, by cleaning
in hemodialysis or administering ethanol, Fomepizole.
Hemodialysis treatment removes the methanol and his metabolites from the circulation,
reducing the shelf life. This is preferable to peritoneal dialysis as it results in more rapid
clearance. Further, ethanol is a treatment form that competitively inhibits the metabolism
of methanol by alcohol dehydrogenase. The affinity of the enzyme for ethanol is 10 to
20 times higher than that of methanol, thus avoiding the formation of toxic metabolites.
In the ethanol administration schedule, the goal is to maintain serum levels between 1
and 1.5 g/L. It should be administered as a bolus loading dose of 0.6 g/kg followed by a
maintenance dose of 66–154 mg/kg/h. IV administration of ethanol is safer than oral
administration, although it can produce irritation and thrombophlebitis.
There is also the 4-methylpyrazole (4-MP) (fomepizole) antidote, which acts similarly to
ethanol by competitively inhibiting ADH. The advantages with respect to ethanol are
various, and its affinity for the enzyme is higher. It has a long half-life (meaning a long
duration of action and dosing convenience), and it does not require continuous
monitoring of plasma levels. It has fewer side effects. Its use in children has been
described in [6, 7].
The purpose of this paper was to report the possibility of poisoning of children with
accidental ingestion of methanol in perfumes and other household products that may
contain this substance.
References
1. J. M. Beno, R. Hartman, C. Wallace, D. Nemeth, and S. LaPoint, “Homicidal
methanol poisoning in a child,” Journal of Analytical Toxicology, vol. 35, no. 7, pp.
524–528, 2011.
2. J. C. van Gaal, R. Petru, and L. T. J. Sie, “An infant with unexplained
epilepsy,” Nederlands Tijdschrift voor Geneeskunde, vol. 154, Article ID A2420,
2010.
3. J. H. Liisanantti, T. I. Ala-Kokko, T. S. Dunder, and H. E. Ebeling, “Contributing
factors in self-poisoning leading to hospital admission in adolescents in Northern
Finland,” Substance Use and Misuse, vol. 45, no. 9, pp. 1340–1350, 2010.
4. U. Celik, T. Celik, A. Avci et al., “Metabolic acidosis in a patient with type 1
diabetes mellitus complicated by methanol and amitriptyline
intoxication,” European Journal of Emergency Medicine, vol. 16, no. 1, pp. 45–
48, 2009.
5. A. H. B. Wu, T. Kelly, C. McKay, D. Ostheimer, E. Forte, and D. Hill, “Definitive
identification of an exceptionally high methanol concentration in an intoxication of
a surviving infant: methanol metabolism by first-order elimination
kinetics,” Journal of Forensic Sciences, vol. 40, no. 2, pp. 315–320, 1995.
6. N. de Brabander, M. Wojciechowski, K. de Decker, A. de Weerdt, and P. G.
Jorens, “Fomepizole as a therapeutic strategy in paediatric methanol poisoning.
A case report and review of the literature,” European Journal of Pediatrics, vol.
164, no. 3, pp. 158–161, 2005.
7. P. E. Wallemacq, R. Vanbinst, V. Haufroid et al., “Plasma and tissue
determination of 4-methylpyrazole for pharmacokinetic analysis in acute adult
and pediatric methanol/ethylene glycol poisoning,” Therapeutic Drug Monitoring,
vol. 26, no. 3, pp. 258–262, 2004.
Case Study: Burns

History
 3-year old boy, presents to pediatric ED with mother
 Child can be heard crying inside waiting/patient room has both hands bandaged
and wrapped
 According to mother, unwitnessed event but child likely grabbed grates on an old
wood burning stove.
 Child immediately screamed out, parents grabbed him, and flushed hands under
cool water.
 Wrapped child’s hands in towels and brought to ED
 No other injuries noted
 PMHx: Had orchidopexy for an undescended testicle at 15 months of age,

otherwise healthy.
 Meds: None
 Allergies: Penicillin – Rash
 Immunizations: UTD
 Development: All normal for fine motor, gross motor, and speech
Vitals
 Temp: 36.4
 HR: 154
 RR: 28
 O2: 99% on RA
 BP: 96/52
 Weight: 14.5 kg
 Glucose: Not Done
Physical Exam
 H+N: Normal, no obvious burns or singe to oropharynx or nares
 Cardiac: N S1S2, no murmurs noted
 Resp: AE=AE, no wheeze, no stridor, no obvious increased work of breathing
 Abdo: Soft, non tender with N bowel sounds
 Hands look as follows……
 CR: 1-2 seconds in all digits
 Radial pulses: N
 Still moving all fingers and wrists
 Mom able to convince child to give a thumbs up
Disposition
 Child’s hands covered in ointment containing
 lidocaine/tetracaine + vaseline
 Wrapped in gauze, mother advised to change daily with
 daily application of ointment
 Given follow up appointment with plastics because of
 location of burn
 Child happy and eating popsicle on way out of the
 department.
Introduction to Burns
 Relatively common injuries caused by direct or indirect
 contact with heat, electrical current, radiation, or
 chemical agents
 With thermal burns, the severity of injury is dependent
 on length of exposure, the temp, and the intrinsic
 tissue structure leading to heat conductivity
 Common denominator in burn injuries is protein
 denaturation and cell death (either by necrosis or
 apoptosis)
Epidemiology
 In the U.S. there are approx 450 000 medical visits per year related to burns, with
3500 deaths and 45 000 admissions.
 The majority of burns occur from fire or flame (44%), scalds (33%), contact with
hot objects (9%), electricity (4%), or chemical agents (3%)
 More than 1/3 of admissions have >10% TBSA affected. Other admission
typically involves severe burns to vital areas such as the hands, face, or feet, or
there has been other trauma involved
 Half of patients are between 19 and 44 years of age. Most commonly affected
are the upper extremities (44%), lower ext. (26%) and H & N (17%)
Pathophysiology
 Unique, dynamic injuries in that there tends to be progression in depth and size
occurring AFTER the time of injury.
 Temperatures below 440 C are generally tolerated without injury. However, as

temperature rises there is an exponential decrease in the time to injury.
 Traditionally burns are separated into 3 concentric zones: Coagulation,

Stasis/Ischemia, and Hyperemia.
 The cont’d progression of burn injuries is multifactorial and not completely

understood at this time.
 The initial inflammatory response triggers a cascade that seems to cause further
injury
 There is an occlusion of the dermal microcirculation with a combination of red

blood cells, neutrophils, and micro thrombi that results in reduced perfusion.
 Inhalation injury: Exposure to heat can cause rapid and extensive upper airway
edema in burn patients.
 Components of smoke such as incomplete combustion materials (ie CO,

cyanide, aldehydes, and oxides) can result in further pulmonary edema and V/Q
mismatch
 Necrosis in the airway leads to de-epithelization and formation of

pseudomembranous casts that cause further airway obstruction
 Reduced ability to clear secretions causing further exacerbation
Classification of Burns
 Burns are classified by mechanism of injury, depth, extent, and associated

injuries and comorbidities.
 First Degree: Limited to the epidermis, characterized by erythema and pain
 Second Degree/Partial Thickness: Can be further subdivided into superficial

and deep. Superficial thickness burns are limited to the papillary dermis while
Deep extend to the reticular dermis.
 Important to distinguish between the two as Deep partial thickness burns will
often will not heal in 2-3 weeks and can lead to scarring and contractures.
 Third Degree: Also referred to as full thickness burns

 Appear thick, white, or tan. Also appear dry with possible charred appearance.
 Non-blanching, and because of nerve destruction are not painful
 Fourth Degree: Extend through the skin into muscle and bone.
 Appear stiff, charred, with visibly thrombosed vessels
Burn Assessment
 Various tools and modalities to assess the depth and healing capacity of burns.
In the emergency department however one must use clinical assessment and
estimation, which can be unreliable.
 The extent of the burned area or total body surface area (TBSA) burned is also
critical in assessment.
 Helps guide the fluid resuscitation management in the patients. Also helps
convey criteria for admittance to the hospital/burn ward.
 Only second degree or deeper burns are used when assessing TBSA affected.
 A useful tool for assessment of smaller burns or scattered areas of burn is that
the area of a patient’s palm and fingers is approximately 1% TBSA
 For larger burns the “rule of 9’s” is frequently employed.
 The rule of nines should not be used for children as their head is larger and, in
proportion, their extremities are smaller than those of adults.
 Finally, burns are classified by severity into minor, moderate, and severe based
on the TBSA burned, the percentage of full-thickness injury, and the involvement
of specific areas such as the face, hands, feet, or perineum.
Pre-Hospital Management
 First priority is to stop the burning process and prevent further injury
 Following this, one should assess the airway, cardiac, and peripheral perfusion
status
 Prehospital administration of fluids is warranted in extensive burns if IV access

can be established effectively and expeditiously in non-burned skin
 Ringers Lactate is the fluid of choice as it reduces the chance of developing

hyperchloremeic acidosis compared to NS. Parkland formula can be used for
dosing
 Burn should be covered with a clean sterile dressing. Minimize hypothermia
ER Management
 People tend to focus on the burns when patients come in, it is important to look
for other injuries and do proper ABC assessment.
 Airway injury and compromise warrants intubation, possibly fiberoptically. If RSI

isn’t possible, consider surgical airway
 If IV hasn’t been established then do so. May need central line if peripheral line
not possible. Humidified O2 should be done to keep sats high (>92%)
 Full monitors should be in place, and a catheter may be placed in order to

monitor U/O
Inhalation Injury
 Smoke inhalation affects 5-35% of burn patients. Presence of inhalation injury

more than doubles the mortality rate in adults.
 Traditional methods for assessment of inhalational injury were/are external

physical exam, however now it is felt that direct visualization via laryngoscopy
(fiberoptic) or bronchoscopy is best.
 Mechanical ventilation helps provide support, can help with secretion control and
help in the recruitment of alveoli.
 Aerosolized NAC and Heparin can help with breakdown of thick secretions while
suctioning and chest physio augment their removal
Fluid Resuscitation
 Prior to WWII many burn patients died of hypovolemic shock and renal failure.
Following combat as well as other fires there began to be fluid regimens.
 The massive amounts of inflammatory mediators lead to increased permeability

of the local and systemic vasculature and extravasation of intravascular fluids
 Patients with small burns can usually be treated with oral fluids (if they can
tolerate oral fluids).
 Patients with severe burns require IV fluids in order to prevent shock and
increase intravascular volume
 Parkland Formula: TBSA x weight (kg) x 4 (ml )Gives the amount of fluid to give
in 24 hours. First ½ should be given in the first 8 hours while the second ½
should be given over the following 16.
 Other formulas can also be used including “rule of 10”
 This formula states that the estimated burn size (percent of TBSA) is multiplied
by 10 to derive the initial fluid rate in milliliters per hour. For every 10 kg above 80
kg, 100 mL is added to this rate
 These regimens are guidelines and fluids should be adjusted according to

tissue/organ perfusion
 Special Considerations: Children have a larger TBSA relative to weight when

compared with adults and therefore have larger fluid requirements
 Fluid needs often calculated on TBSA rather than weight, using things such as
the Galveston Formula.
 Colloids: Since leakage of proteins through capillaries lasts 12-24 hours,

colloids are not generally recommended in the initial resuscitation unless the
burn is very deep.
 ABA guidelines consider the possible addition of colloids AFTER the 12-24 hr
mark to decrease fluid requirements
Local Wound Care
 Burns should be considered contaminated and have gentle cleansing with soap
and cool water. Necrotic tissue should be carefully removed as needed
(analgesia will most likely be warranted in these scenarios)
 Tetanus booster should be given if patient has not had booster in the last 5 years.
 Ice water should generally be avoided as it has been associated with increased
tissue injury and hypothermia
 Burn Blister Management: Remains a topic of debate. Some evidence that

there is less infection with intact blisters, however tends to be less pain with
ruptured blisters.
 With blisters that have already ruptured, any necrotic epidermis should be gently
removed while adherent epidermis is left intact. With large or tense blisters, the
unruptured blister may be aspirated with a sterile needle
Burn Dressings
 Purpose is to protect the wound, to reduce pain, to absorb wound exudate, and
to reduce evaporative heat loss
 First degree wounds can generally be managed with topical anesthetics, aloe
vera gels, and NSAIDS
 Second degree wounds can be managed with dressings with the main principle
being CLEAN AND GREASY!
 Open: Appropriate for large, contaminated burns with exudate.
 The wound can then be covered by a non-occlusive dressing with daily cleansing
and dressing changes.
 Closed: Use of occlusive dressings for a moist environment in a wound that has
little to mild exudate.
 Saran Wrap can be used as it seals in heat, acts as a barrier and also allows you
to visualize the wound.
Pain Management
 Burn injuries are among the most painful experienced and pain control should be
among the highest priorities for physicians
 Pain, especially in the emergent phase can be divided into three categories:
background, breakthrough, and procedural.
 Pharmacologic agents used to treat burn pain include opioid analgesics,

nonopioid analgesics, anxiolytics, and anesthetics. The type of medication used
is determined by the severity of pain, the anticipated duration of pain, and
intravenous (IV) access
 Minor burns can be managed with Tylenol and NSAIDS
 In the emergent setting moderate to severe burn pain is generally managed with
parenteral opioids titrated to effect.
 Fentanyl (with a short half-life) can be used for short breakthrough and
procedural pain for things like debridement and dressing changes
 Intravenous infusion of lidocaine (1 mg/kg followed by 40μg/kg/min infusion) has

also been shown to reduce the pain in burn patients.
 In large severe burns or pediatric burns consider sedation and regional nerve
blocks
References
 Rosen’s Guide to Emergency Medicine
 UpToDate
 American Burn Association Guidelines
Case Study: Witnessed Arrest With Bystander

CPR
Abstract
A 57-year-old physician in a large metropolitan area in Israel collapsed suddenly. An
ambulance was dispatched after a call to EMS (see timeline). Two bystander physicians
began immediate compression-only CPR, and the patient regained consciousness.
Timeline of Events
17:57 Call to EMS
17:58 Ambulance leaves station
18:06 Ambulance arrives on scene
18:39 Ambulance leaves scene for hospital
18:45 Ambulance arrives at hospital
After a few seconds the patient collapsed again, and compression-only CPR was
restarted. The mobile intensive care unit (MICU) dispatched to the scene included four
team members: two paramedics, one EMT and a paramedic student. It arrived in less
than 10 minutes after the EMS call. The physicians on scene continued delivering
compressions until EMS arrived.
EMS found the patient gasping, and immediately one of the team members replaced the
physician performing compressions, while another ventilated the patient with a bag-
valve device connected to oxygen. The patient was found to be in ventricular fibrillation
(VF). A 200-joule biphasic shock was delivered, and BLS continued with minimal
interruption while a mechanical compression device (LUCAS 2) was attached to the
patient. No medical history for this patient was available on scene.
At this time the patient, still in VF, began moving his hands toward the compression
device and grabbed it. While the compressions were paused for ventilation, the patient
became flaccid again until the device delivered another compression. The team decided
not to intubate the patient, since his level of consciousness indicated it would not be
possible without sedation, and concentrated on the quality of BLS delivery.
Efforts to gain vascular access became difficult since the patient had folded his hands
and would not allow the paramedics to straighten them. BLS continued without
interruption for a total of three rounds of two minutes each, with a total of three 200-
joule shocks every two minutes. Without vascular access, no epinephrine was
administered, and the airway was managed with an oropharyngeal airway (tolerated for
most of the time) and the bag-valve device. At this time the paramedics did not know if
sedation by administration of midazolam, etomidate or ketamine was possible for a
patient in cardiac arrest, since this situation was never before discussed or
encountered. Eventually the paramedics obtained vascular access via an intraosseous
device to the left tibia and continued CPR. The patient maintained purposeful
movement.
After three shocks and six minutes of CPR, the patient achieved ROSC, and his heart
rhythm changed to ventricular tachycardia. Two synchronized shocks were delivered
until the rhythm changed to sinus tachycardia with a corresponding pulse. At this time
the patient became restless, and the crew administered IO midazolam. The patient was
hemodynamically stable, and the electrocardiogram showed no signs of ischemia, ST
elevation or other changes suggesting a reason for the cardiac arrest. The nearest
hospital’s intensive cardiac care unit advised transport to the ER. On the short ride to
the hospital, the patient woke up and was fully aware of what had happened.
At the Hospital
The patient was admitted to the emergency department and transferred to the ICCU.
His medical history included rheumatic heart disease, dyslipidemia, a history of
smoking, and mechanical aortic and mitral valve replacement. In the last year the
patient had experienced a few episodes of paroxysmal atrial fibrillation but was
functioning normally, including doing daily exercise. After admission he had no episodes
of chest pain, his ECG was normal, and he showed no electrolyte imbalances or QT
changes.
The patient’s heart echocardiogram demonstrated new heart failure—a significant

change for the worse since his last echocardiogram in 2012, following a mitral valve
replacement. The patient’s cardiac coronary computed tomography angiogram (CTA)
demonstrated hypertrophy of the septum and a nonrestrictive disease in his coronary
arteries. Surgeons implanted a cardioverter-defibrillator, and the patient was released
from the hospital with no neurological damage.
Discussion
While mechanical compression devices have become common in prehospital and
hospital treatment, there are no current clinical guidelines for treating patients who
regain consciousness during cardiac arrest. This phenomenon presents an interesting
challenge for healthcare providers who are not used to treating responsive patients
while performing CPR during such arrests. Some of the procedures that are usually
performed (such as obtaining vascular access or intubation) require the patient to be
unconscious, or at least to not resist treatment.
Currently, cardiac arrest drugs are limited to those intended to restore circulation
(vasopressors, antiarrhythmics). The use of mechanical compression devices presents
a new challenge that may indicate sedation of patients. Analgesic medications should
be selected for minimal cardiovascular influence. Drugs that are currently being used in
EMS systems for sedation, analgesia and anesthesia include:
Short-acting benzodiazepines like midazolam and long-acting benzodiazepines like

Assival;
Ketamine—for sedation, analgesia and anesthesia;
Etomidate—for general anesthesia and sedation;
Opioids—morphine and fentanyl for analgesia and anesthesia.
We suggest using fentanyl or ketamine for patients who gain some level of
consciousness while a mechanical compression device is working.
Fentanyl is a synthetic opioid that is becoming common in EMS systems, as it has

sedative and analgesic but minimal cardiovascular effects. While today in some
systems it’s administered intranasally for safety reasons, drugs in cardiac arrest should
be administered through an intravenous or intraosseous catheter according to current

guidelines and since intranasal absorption is probably diminished in cardiac arrest.
Ketamine is also a common drug that can provide analgesia and sedation with minimal
cardiovascular effects and be used via the IV or IO route.
As mechanical compression devices gain popularity in EMS systems, research in this

area should be conducted so clear guidelines can be published and practiced in
hospitals and, especially, in prehospital settings.
References
1. Neumar RW, Otto CW, Link MS, et al. Part 8: Adult Advanced Cardiovascular Life
Support—2010 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care. Circulation, 2010 Nov 2;
122(18 Suppl 3): S729–67.
2. Meaney PA, Bobrow BJ, Mancini ME, et al. Cardiopulmonary resuscitation
quality: improving cardiac resuscitation outcomes both inside and outside the
hospital: a consensus statement from the American Heart Association.
Circulation, 2013 Jul 23; 128(4): 417–35.
3. Rubertsson S, Lindgren E, Smekal D, et al. Mechanical chest compressions and
simultaneous defibrillation vs. conventional cardiopulmonary resuscitation in out-
of-hospital cardiac arrest: the LINC randomized trial. JAMA, 2014; 311(1): 53–61.
4. Dallan LA, Vargas TT, Janella BL, et al. Mechanical devices are more effective
than manual compressions regarding resuscitation concomitant with emergency
percutaneous coronary intervention in cardiac arrest. Circulation, 2014;
130(Suppl 2): A100.
5. Stub D, Bernard S, Pellegrino V, et al. Refractory cardiac arrest treated with
mechanical CPR, hypothermia, ECMO and early reperfusion (the CHEER trial).
Resuscitation, 2015; 86: 88–94.
6. Wik L, Kiil S. Use of an automatic mechanical chest compression device
(LUCAS) as a bridge to establishing cardiopulmonary bypass for a patient with
hypothermic cardiac arrest. Resuscitation, 2005; 66(3): 391–4.
7. Mateos-Rodríguez A, Pardillos-Ferrer L, Navalpotro-Pascual JM, et al. Kidney
transplant function using organs from non-heart-beating donors maintained by
mechanical chest compressions. Resuscitation, 2010; 81(7): 904–7.
8. Bihari S, Rajajee V. Prolonged retention of awareness during cardiopulmonary
resuscitation for asystolic cardiac arrest. Neurocritical Care, 2008; 9(3): 382–6.
Case Study: Effective Cardiopulmonary

Resuscitation In a Pregnant Woman
Abstract
The management of cardiac arrest in pregnancy is an important task for the emergency
physicians. Some reasons for cardiac arrest are reversible and should be recognized
and managed promptly. Cardiopulmonary resuscitation follows general advanced
cardiac life support guidelines with several modifications for pregnant women, taking
into account the lives of both mother and fetus. Here, we present the case of 23-year-
old pregnant patient who came to Guru Nanak Dev Hospital, Amritsar; in shock, had a
cardiac arrest, successfully resuscitated in Intensive Care Unit (ICU), delivered by
emergency cesarean section and was discharged from ICU on 9th day in healthy state.
Keywords
 Cardiac arrest
 cardiopulmonary resuscitation
 cesarean section
 pregnancy

Introduction
The cardiac arrest in pregnancy is very rare with an occurrence of one case in every
30,000 patients. Various causes of cardiac arrest in pregnancy are amniotic fluid
embolism, hemorrhagic shock, eclampsia, pulmonary thromboembolic events, sepsis,
anaphylaxis, trauma, congenital, and acquired cardiac diseases. It is estimated that the
survival rate for in-hospital cardiac arrest varies from 0% to 42% and the most
commonly seen in only 15–20% cases. When a pregnant women's heart stops two lives
are threatened. There are increased chances of cesarean section in them for the
survival of mother/child or both. Favorable outcome is seen with effective and early
cardiopulmonary resuscitation (CPR).
Case report
A 23-year-old G2P1L1, at 28 weeks gestation with previous normal vaginal delivery was
brought to emergency labor room in a state of shock. Blood pressure (BP) and pulse
were unrecordable at the time of admission. The patient was unconscious and fetal
heart sound was also unrecordable. History was derived from the relatives, and there
was a history of amenorrhea since 7 months and bleeding per vaginam for the last more
than 24 h. There was no any history of drug abuse or alcohol intake. We could not
extract much obstetrical history as the attendants were illiterate and antenatal check-up
was also missing. Before admission in our hospital, she remained admitted in three
different private hospital for treatment, but was not treated for bleeding per vaginam
anywhere. Immediately, a large bore intravenous (i.v) cannula was secured and i.v
fluids in the forms of colloids and crystalloids were started. All the relevant samples
were sent to investigate the case. Foley's catheter was put to measure hourly urine
output, and urine was also sent for albumin, which came out to be negative after
laboratory test. All electrolytes were within normal limits. Her blood sugar level was 84
mg%. Emergency ultrasound showed absent fetal heart. As the patient was in shock, so
it was decided to shift the patient to Intensive Care Unit (ICU) as there was no
immediate need for hysterotomy since fetus was already dead and our main
consideration was to save the mother now. As the patient was being shifted from the
stretcher to bed, the patient had a sudden cardiac arrest in labor room itself.
Immediately, wedge was kept under the right hip, and chest compressions were started
as per advanced cardiac life support (ACLS) guidelines that are, 100 compressions/min.
The simultaneously patient was intubated with endotracheal tube number 7 fixed by
another rescuer and tube was secured. Rescue breaths were given with AMBU at
12/min. Injection adrenaline 1 mg i.v was given twice and all others resuscitative
measures were taken. The patient was revived within 4 min of CPR. Inotropes were
started to maintain BP with dopamine at 10 µg/kg and noradrenaline at 1610 µg/kg.
Then the patient was shifted to ICU and put on synchronized intermittent mandatory
ventilation volume control (SIMV-VC) mode of ventilator with following settings FiO2:
100%, tidal volume (TV): 500 ml, positive end expiratory pressure (PEEP): Off, positive
support ventilation (PSV): 15. Patient's vitals on ICU admission were as follows: BP
92/60 mmHg on the right side of the arm, pulse rate (PR): 120 bpm, SPO2: 95%. The
patient was managed with 4 whole blood and both the vasopressors continued. As the
patient's BP started rising, the patient had the second bout of bleeding per vaginam. P/A
examination was done by the obstetrician and uterus was measured at 28 weeks,
oblique lie. In the meantime, recent ultrasound scan was brought by attendants, which
showed Grade 4 placenta previa (placenta completely covering internal os). After proper
consent, the patient was shifted to operation theater with following vitals BP 100/64 on
dopamine 1010 µg/kg and noradrenaline 1610 µg/kg, PR 128 bpm and an emergency
lower segment cesarean section (LSCS) was performed under general anesthesia. The
patient was given i.v 80 mg ketamine, 4 mg vecuronium and isoflurane and dead baby
extracted out as breech. Placenta that was already lying separated was removed.
Uterus was closed in layers. Intraoperatively, 3 whole blood transfusions, 1 L Ringer
lactate and 4 fresh frozen plasma were transfused. Now blood samples were taken and
sent for laboratory examination again. The patient stood the surgery well and was
shifted back to ICU and put on ventilator SIMV-VC mode with following settings FiO2:
50%, TV: 500 ml, PEEP: 3, PSV: 15. The patient remained stable with vitals BP 120/72
mm Hg, PR 115 bpm, and SpO2 95%. The patient was intensively monitored in ICU.
Inotropes were tapered off in next 4 days. The patient regained consciousness and
responded to verbal commands and was weaned off from the ventilator on 7th day. She
was shifted to the ward on 9th day and the subsequently discharged with intact
neurological functions.
Discussion
Resuscitation of pregnant women is a challenging process as there are various
anatomical and physiological changes that are, decrease in respiratory reserve volume.
Furthermore, there is difficult airway resulting from pharyngeal edema, increased risk of
aspiration due to relaxation of the esophageal sphincter, decreased effect of chest
compressions as a result of decreased venous return leading to supine hypotension and
obstruction of forward flow of blood by the gravid uterus, especially in cardiac arrest.
There are two lives at stake; mother and fetus. The correct and fast decision of the
resuscitator leads to better survival rates of both mother and fetus. Early restoration of
the maternal circulation should be there in order to increase the survival rate of the
fetus. In the present case, study fetus was already dead on admission. In India and
other developing countries, most of the ignorant patients do not go for proper antenatal
check-up despite government policies to give free treatment to patients to decrease
infant mortality rate and mother mortality rate. Successful CPR implies that early
recognition of cardiac arrest, aortocaval decompression, early hysterotomy, or cesarean
section, and reversing the cause of cardiac arrest. According to ACLS guidelines
mother's circulation should be restored within 5 min else emergency hysterotomy is to
be done. Since our patient was revived in <5 min and fetus had already expired so
patient was first stabilized in ICU and cause of arrest was identified and treated, that is,
hemorrhagic shock and then LSCS was performed.
Antepartum hemorrhage complicates about 2–5% of pregnancies, out of which one-third

is due to placenta previa. It accounts for 25% of maternal deaths in pregnancy. Rapid
assessment and initiation of appropriate resuscitative measures can greatly improve
prognosis. Placenta previa is abnormal implantation of placenta in the lower uterine
segment. Thus, an accurate and early diagnosis of placenta previa is important and
useful in clinical obstetrical practice. However, the technology advances in
ultrasonography, the diagnosis of placenta previa is commonly made earlier in
pregnancy. Transvaginal ultrasonography is most sensitive and specific for diagnosis. If
the bleeding is minimal, and fetal reassurance is noted, then expectant management
may be considered. However, if bleeding or contractions occur, the patient must rapidly
go to the hospital for evaluation and testing. If the bleeding persists and is heavy,
preparation for immediate emergency LSCS is indicated. As in the present case, there
was an oblique lie, preterm pregnancy with intra uterine device and bleeding per
vaginam, so emergency LSCS was done.
Conclusion
Cardiac arrest is a rare, unexpected and devastating event for pregnant patients, as
well as doctors who treat them. Early anticipation and treatment of various pathologies
in pregnant women may prevent cardiac arrest. A multidisciplinary team should be
familiar with ACLS guidelines and their modification in pregnant women. It should also
be kept in mind that there is no change in doses of medication or defibrillator in the
resuscitation of pregnant women. However, as the pregnant patients have decreased
functional residual capacity and increased oxygen demand, they develop hypoxemia
very rapidly, so prompt and excellent CPR with some modifications should be started
immediately. Proper co-ordination among the anesthesiologists, obstetrician, medical
specialist and intensive care specialist is very important.
Conflicts of interest
There are no conflicts of interest
References
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Case Scenario: Perioperative Airway Management of a Patient with Tracheal Stenosis
TRACHEAL stenosis is a rare but a life-threatening condition and is caused by

congenital problems, postintubation injury, trauma, tracheal tumor, and compression of
the trachea by tumor. Although accurate prevalence of this condition is unknown, an
incidence of 4.9 cases per million per year is estimated for postintubation tracheal
stenosis.1A stenosis commonly occurs at the cuff of the tube (intrathoracic trachea) or
at the level of the tracheostomy stoma (extrathoracic trachea).
Anesthesia of a patient with tracheal stenosis is challenging for anesthesiologists.
Depending on the severity and location of the stenosis and the type of surgical
procedure, there may be a variety of choices for perioperative airway management such
as a facemask, laryngeal mask airway,2an tracheal intubation tube,3,4cardiopulmonary
bypass,5and extracorporeal membrane oxygenation.6The American Society of
Anesthesiologists practice guidelines for management of the difficult airway primarily
focus airway problems caused at the extrathoracic airway and may not be helpful,
particularly for managing patients with intrathoracic tracheal stenosis.7In this case
scenario, we present a patient with severe intrathoracic tracheal stenosis, who required
surgery for a lumbar fracture in the prone position. Various airway management
strategies and the actual management used are discussed.
Preoperative Information of the Case
A 38-yr-old obese man (height, 172 cm; weight, 95 kg; body mass index, 32 kg/m2) was
scheduled to have a thoracolumbar laminectomy and fixation for a burst fracture of the
first lumbar vertebra. Surgery was to be performed in the prone position. The operation
duration and blood loss were preoperatively estimated to be 4 h and 500 ml. He had a
history of prolonged intubation when he suffered a traumatic brain injury at 8 yr of age.
He had epilepsy treated with phenobarbital but had no impairment of neurologic
development and was cooperative. Despite undergoing tracheal resection and plasty for
severe postintubation tracheal stenosis at 17 yr of age, he had relatively loud inspiratory
and expiratory stridor while awake. Spirometry in the sitting position revealed reduced
forced expiratory volume in the first second (FEV1= 1.95 l, 53%-predicted) and peak
expiratory flow rates (PEF = 180 l/min, 30% predicted). Arterial blood gas analysis
indicated mild impairment of oxygenation but normal ventilation (Fio2= 0.2, pH = 7.43,
Pao2= 71 mmHg, Paco2= 33 mmHg). A flow-volume loop showed a typical upper
airway obstruction pattern (fig. 1). Three-dimensional computed tomography (CT) of the
trachea revealed severe intrathoracic tracheal stenosis more than 3 cm in length. In
cross-section, the stenotic lesion was elliptical with a minor axis of 0.5 cm and a major
axis of 1.5 cm (fig. 2). Despite the tracheal stenosis, he had no dyspnea during daily
activities and was otherwise healthy. Nurses in the ward witnessed loud snoring and
occasional apnea during sleep. Preoperative airway examination revealed Mallampati
class 3, normal thyromental distance, and no limitation of neck or mandible movements.
The orthopedic surgeons considered that neither conservative therapy nor surgery with
regional anesthesia was appropriate because of his neurologic symptoms and the
estimated operational duration and invasiveness of the surgery.
Fig. 1. A flow-volume loop during forced expiration

and inspiration in this case. Note marked reduction in
both PEF and PIF. insp = inspiration; exp =
expiration; PEF = peak expiratory flow rate; PIF =
peak inspiratory flow rate; FEV1= forced expiratory
volume in the first second.
Fig. 2. Tracheal three-dimensional computed

tomography of this case revealed severe
intrathoracic tracheal stenosis over 3 cm in length
(arrows ) and elliptical airway shape with a minor
axis of 0.5 cm and a major axis of 1.5 cm.
Airway Management Plans by Airway Experts

Only the preoperative information with the figures described above was initially sent to
both Drs. Asai and Cook. They were selected because of their previous reports of
similar cases.3,4The following are their airway management plans for this patient.
Dr T. Asai
I follow an algorithm for anesthetic management of patients with tracheal stenosis
based on its pathophysiology (fig. 3). Although the patient had relatively loud inspiratory
and expiratory stridor and apnea during sleep, he had no dyspnea during daily activities.
Therefore, I consider that spontaneous breathing or mechanical ventilation is likely to be
possible through the stenosis with general anesthesia. Nevertheless, severe airway
obstruction may occur during induction of general anesthesia, and thus the appropriate
backup method will be required to prevent disaster.
Fig. 3. An algorithm for anesthetic

management of patients with tracheal
stenosis. #1: Airway imaging and pulmonary
function test are helpful for this decision
making. #2: Collapsibility or expandability of
the trachea needs to be assessed for this
decision making. GA = general anesthesia;
ET = endotracheal tube; PCPS =
percutaneous cardiopulmonary support.
There are three possible methods for airway management of this case: (1) the use of a
supraglottic airway alone, (2) the use of a supraglottic airway and a tube-exchange
catheter, and (3) the use of a supraglottic airway, an endotracheal tube, and a tube-
exchange catheter such as Cook Airway Exchange Catheter (Cook Medical,
Bloomington, IN; 2.7 mm internal diameter [ID]). The choice of method would depend on
both the risks of airway obstruction or dislodgement of the selected airway device and
accessibility of the airway for reinsertion of the device.
In this case, the airway might be managed with a supraglottic airway alone, but there
are two major potential problems with this method: airway obstruction after induction of
anesthesia and dislodgement of the supraglottic airway (particularly when the patient is
turned to prone position from the supine position). One possible solution is to place the
patient in the prone position and insert a supraglottic airway while the patient is still
awake, and then induce anesthesia with increasing concentrations of sevoflurane while
maintaining spontaneous breathing. Although the presence of the supraglottic airway
would prevent airway obstruction above the vocal cords, worsening of the tracheal
stenosis and hence severe airway obstruction may develop during inhalational induction
with sevoflurane. In such a case, administration of sevoflurane should be terminated
and the patient should be woken up. If inadvertent dislodgement of the airway device in
the prone position is a risk, safety would be increased by prior insertion of a tube-
exchange catheter, because this would enable both the maintenance of oxygenation
until reinsertion of the supraglottic airway and the tracheal intubation through it.4,8
Alternatively, a more conservative but a safer approach, which I consider the most
appropriate in this case, is tracheal intubation with the two backup methods of the use
of both a supraglottic airway and a tube-exchange catheter. In this case, the narrowest
caliber of the trachea is 5 mm, and thus the largest size of an endotracheal tube, which
can be passed through the stenosis, would be 4.0 mm ID, and ventilation may not be
sufficient. Therefore, it would be necessary to insert a larger endotracheal tube with its
tip proximal to the stenosis. Three-dimensional CT indicates that the stenosis is in the
mid to lower trachea, and thus it would only be possible to insert the distal 3-4 cm of the
endotracheal tube into the trachea, necessitating backup plans, in case of tube
dislodgement. In such an event, either the supraglottic airway or the exchange catheter
could then be used for maintaining oxygenation and reinserting the endotracheal tube. I
would prepare for jet ventilation through the exchange catheter.
After preoxygenation of the patient in the supine position, I would allow the patient to
breathe increasing concentrations of sevoflurane in oxygen, and then assist ventilation
manually via a facemask. After injection of a neuromuscular blocking agent, I would
insert a Cook airway exchange catheter into the trachea under direct laryngoscopy, and
then insert either the ProSeal Laryngeal Mask Airway ™ (PLMA ™; Laryngeal Mask
Company, Henley-on-Thames, United Kingdom) #5 or i-gel (Intersugical Ltd.,
Wokingham, Berkshire, United Kingdom), another supraglottic airway, while the
exchange catheter is placed outside the supraglottic airway. With the aid of a fiberoptic
bronchoscope, I would pass a reinforced endotracheal tube through the supraglottic
airway into the trachea so that the tip of the endotracheal tube is approximately 1-2 cm
proximal to the stenosis. I would not inflate the endotracheal tube cuff, because it would
be positioned at the glottis. Wrapping adhesive tape around the endotracheal tube at
the connecter of the supraglottic airway would prevent both dislodgement of the
endotracheal tube and gas leakage through the supraglottic airway. I would then adjust
the position of the exchange catheter so that its tip is beyond the tracheal stenosis. After
the patient is turned to the prone position, I would confirm (using a fiberscope) the
appropriate positions of both endotracheal tube and exchange catheter. I would
maintain the tidal volume as low as possible allowing hypercapnia to prevent excessive
peak airway pressure. When possible, spontaneous breathing would be resumed. After
surgery, I would remove the supraglottic airway once the patient has recovered from
general anesthesia and is responsive to verbal commands, but would leave the tube
exchange catheter in place, until it becomes certain that the patient can maintain a clear
airway.
Dr. T. M. Cook
This is a truly difficult patient. I would first reiterate to the surgeons that perioperative
airway complications are a potential risk to the patient's life. The options of conservative
treatment or transfer to a center with facility for combined tracheal reconstructive and
trauma surgery must be explicitly considered.
Assuming neither is possible I would premedicate the patient with a proton pump
inhibitor 12 h before anesthesia. Two experienced anesthetists and an experienced
anesthetic assistant would be required and briefed. I would start by placing a narrow
gauge cricothyroid cannula specifically a 13-gauge Ravussin cannula (VBM
Medizintechnik, Sulz, Germany) with local anesthesia and confirm its position by feeling
expired gas, seeing gas exit through a bubble of saline and with capnography. If there
was concern about the position of the Ravussin cannula, I would perform awake
fiberoptic inspection to confirm its position before proceeding. Next, I would place
a PLMA ™. If the patient was cooperative, I would do this during topical anesthesia. If
he was not I would place it during general anesthesia. I would preoxygenate the patient
fully with continuous positive airway pressure performed with at least 25 degrees head
up position to increase lung volumes and maximize the apnea period before hypoxemia
develops. I would administer a modest dose of opioid (e.g. , fentanyl 100 μg titrated in >
2-3 min) and propofol by target-controlled infusion. I would start with a low propofol
effect site target (1-1.5 μg/ml) and increase this in steps of 0.5 μg/ml for every 1-3 min
while maintaining spontaneous ventilation. At the point of eye closure, but before full
anesthesia, I would assess ease of assisted ventilation. If ventilation was difficult or
impossible, I would abandon this attempt and allow the patient to wake up. After
confirmation of adequate mask ventilation, I would then paralyze with rocuronium,
increase the depth of anesthesia, and insert a PLMA ™, using a bougie-guided
technique.9,10After placement of the PLMA ™, I would then intubate the trachea
through it. If the PLMA ™ was placed awake, I would induce anesthesia after PLMA ™
placement. For intubation, I would use a 4.2-mm fiberscope on which an Aintree
Intubating Catheter (AIC; Cook Medical, Bloomington, IN) was mounted. After passage
of the AIC, I would railroad a 6.5-mm ID intubating Laryngeal Mask Airway ™ (LMA ™)
endotracheal tube over it. If the AIC passed easily, I anticipate that the
intubating LMA ™ endotracheal tube would also pass. If the AIC was tight/snug, I would
pass a Cook airway exchange catheter through the AIC and railroad a 5.0-mm ID
microlaryngoscopy tube over the airway exchange catheter. I would then confirm
position of the endotracheal tube beyond the stenosis. If the AIC could not pass without
undue force, I would ventilate until paralysis was reversed (sugammadex may be useful
here due to its ability to produce rapid and complete reversal of rocuronium paralysis)
and then wake up the patient. During surgery, I would administer 8.0 mg of intravenous
dexamethasone to minimize edema of the stenotic region. At the end of surgery, I would
exchange the endotracheal tube for a Cook airway exchange catheter and a PLMA ™. I
would then assess ease of ventilation (and spirometry) with the patient still
anesthetized. I would then allow the patient to wake and remove the PLMA ™, but not
the exchange catheter. If there was any suggestion of trauma during the intubation or
concern about edema at the time of extubation, I would admit the patient to intensive
care unit for 24-48 h of sedation, ventilation, and steroid to allow airway edema to settle.
Actual Airway Management in This Patient
The history of tracheal surgery and persistent stridor suggested a rigid tracheal wall at
the stenotic region allowing insertion of an endotracheal tube with 5-7 mm outer
diameter, that is, only 4.0-5.5 mm ID without injuring the tracheal wall. We considered
that positive pressure ventilation with such a small diameter tube might be difficult in this
obese patient during surgery in prone position. Furthermore, traumatic insertion and
prolonged placement of a larger diameter tube were considered to be disadvantageous
because of the potential for development of mucosal edema and further narrowing of
the trachea after tracheal extubation. Therefore, we decided not to intubate the trachea,
but to use the PLMA ™ for positive pressure ventilation. The patient agreed with this
strategy after we explained its potential benefits and risks to him.
Because of clinical symptoms and body habitus suggesting potential obstructive sleep
apnea, we performed nocturnal oximetry preoperatively. We calculated 4% oxygen
desaturation index (i.e. , the average number of oxygen desaturations by 4% or more
below the baseline level per hour). Although an oxygen desaturation index greater than
5 h−1is suggestive of sleep-disordered breathing, the index was 3 h −1in this
patient.11Despite the negative result of the sleep study, nasal continuous positive
airway pressure was prescribed because this could help maintain tracheal patency both
for treatment of his snoring and in case of mucosal edema at the tracheal stenosis
developed after surgery. The patient tolerated this treatment well.
General anesthesia was induced with intravenous administration of remifentanil,
propofol, and vecuronium, and a PLMA ™ (#5) was inserted, guided by a gum elastic
bougie. Anesthesia was maintained with inhaled sevoflurane and an infusion of
intravenous remifentanil. With pressure-controlled ventilation during surgery (peak
inspiratory pressure 22 cm H2O, positive end-expiratory pressure 7 cm H 2O, respiratory
rate 8 breaths/min, inspiratory expiratory ratio 1:3) through the PLMA ™, we saw no
signs of high airway resistance or airflow limitation such as low tidal volume or lack of
formation of an alveolar plateau on capnography (tidal volume 730 ml, end-tidal CO 231
mmHg). The surgery was uneventfully accomplished. The PLMA ™ was removed when
the patient was fully aroused. Optimal postoperative analgesia was achieved by
intravenous injection of nonsteroidal antiinflammatory drug and a continuous

intravenous infusion of fentanyl. After the patient arrived on the ward, nasal continuous
positive airway pressure with oxygen was applied immediately and was continued for
three postoperative nights. This was effective in eliminating both snoring and stridor
during sleep.12He did not complain of dyspnea after surgery and was discharged fully
mobile.
Comments by the Airway Experts

on Perioperative Airway Management
 Dr. T. Asai
I believe that preoperative assessment and anesthesia management of the case

described are generally reasonable and accord with my assessments and plans.
The preoperative respiratory state during wakefulness and sleep was sufficiently
assessed, and the visual assessments of the stenotic region with three-dimensional
CT imaging of the trachea in addition to chest radiographs were informative. These
meticulous assessments may certainly be useful to plan a safer anesthesia
management (providing that the time and cost can be spent). Nevertheless, caution
may be required, because the absence of significant airway obstruction during sleep
does not guarantee that there will be no airway obstruction during anesthesia.
There have been several reports of complete airway obstruction in patients with
mediastinal masses, without any preoperative signs of airway obstruction.13In this
case, the three-dimensional CT and preoperative assessments suggest that
complete airway obstruction is unlikely, but it might have been safer to induce
anesthesia by inhalation of increasing concentrations of a volatile anesthetic (such
as sevoflurane) and then to give a neuromuscular blocking agent after confirming
that no airway obstruction has occurred.
There may be two major possible problems with the anesthesia management
performed by Drs. Isono and Kitamura. First, air trapping may occur beyond the
stenosis, when the ventilation is controlled. This can be reduced by decreasing the
inspiratory/expiratory ratio (that is increasing the expiratory time). In this case,
because the stenosis had a minimally acceptable caliber, the pressure-controlled
ventilation worked well, and sufficient ventilation volume was obtained.
Spontaneous breathing might have been a better choice if ventilation had been
insufficient during controlled ventilation.
Another possible problem is that the use of the PLMA ™ alone might have become
difficult if (although not likely in this case) the device had been inadvertently
dislodged or airway obstruction at the stenotic region had occurred. If there are
concerns about access to the patient's face, or about a prolonged operation time, I
would use a backup method of leaving a tube-exchange catheter beyond the

stenosis and possibly an endotracheal tube with its tip proximal to the stenosis.
Postoperatively, nasal continuous positive airway pressure, known to minimize
airway obstruction, was applied for three postoperative nights. Because tracheal
intubation seemed not difficult, the choice of applying nasal continuous positive
airway pressure postoperatively seems better than my plan of leaving a tube
exchanger to the trachea after operation.
 Dr. T. M. Cook
For each possible solution that is explored, several potential complications arise. I will
limit myself to answering the following specific questions. I do not know whether my
plans would work: Drs. Isono and Kitamura have the massive advantage of knowing
their plans did! In many respects what matters most in this case is not what plan A is,
but how the anesthetist plans to respond if plan A fails immediately or mid-surgery. It is
essential for the anesthetist to have a plan B, as a minimum, before induction of
anesthesia.
How Do I Assess the Problem?
My first consideration is that all aspects of this patient's care potentially put him at risk.
His features offer the possibility of supraglottic and subglottic problems leading to both
difficult mask ventilation and difficult intubation.14Hypoxemia will be rapid and severe if
the airway is lost in this obese patient who will have a limited functional residual
capacity. Passage of a tube beyond his tracheal narrowing may be the most
problematic.
However, there are two patient features that I find reassuring. First, the fact that the
tracheal narrowing (although only 5 mm in its minor diameter) is 15 mm in its major
diameter suggests strongly to me that it will admit a larger endotracheal tube than one
with an external diameter of 5 mm. The trachea is a dynamic and nonrigid structure, and
anyone who has observed tracheal dilation will confirm that it will often accept a larger
diameter tube than its resting dimensions. Second, the fact that the patient suffers no
limitation to his daily activities indicates that gas flow is considerably better than some of
the patient's features suggest.
Why Do I Believe This Patient Needs Intubation?
I did consider use of the PLMA ™ as the primary airway throughout anesthesia.
The PLMA ™ is my “go to” airway and I have extensive experience with it for both
routine15and difficult airway management.16Such is my confidence in it that I have
abandoned use of the LMA-Classic ™ (Laryngeal Mask Company), because I believe
that its performance and safety profile is inferior to that of the PLMA ™. Despite this, I
rejected its use for this case because I was concerned that if it failed with the patient in
the prone position, rescue would be hazardous and might fail with fatal consequences.
I did not consider the option of use of PLMA ™ with an airway exchange catheter in
place through the vocal cords in case rescue was required. This is ingenious and adds
a level of safety. Despite this, if I was required to anesthetize this patient I would still
advocate tracheal intubation before commencing a 4-h procedure in the prone position.
I have used the PLMA ™ myself in approximately 10 patients in the prone position and I
am aware that it has been used in several series of patients in the prone
position.17,18However, the patients enrolled in these studies were at low risk and the
largest series is 245 patients17: airway obstruction occurred in three patients (>1%). In
contrast, the patient in this case has an increased risk of problems with both ventilation
and oxygenation. Minor degrees of misplacement and airway swelling during surgery in
the prone position would likely lead to airway obstruction. If airway obstruction occurred
in this patient, hypoxia would likely be rapid and profound. His airway is likely difficult to
manage in the supine position in ideal circumstances. Despite my experience, I would
be concerned that problems occurring in the prone position, mid-surgery would be so
difficult to manage that the patient's life would be at risk. Despite the difficulties posed
by intubation (and extubation), I would chose tracheal intubation in this case.
Why Do I Induce with Incremental Target-controlled Infusion Propofol?
Most anesthesiologists, performing spontaneous breathing induction of anesthesia,

reach for a volatile agent. With the experience of both, I have a strong preference for
use of a slowly increasing, incremental dose of target-controlled propofol, while
maintaining spontaneous ventilation. There are only limited descriptions of this
technique.19,20The main advantage of incremental target-controlled infusion of
propofol over rapid intravenous induction is that spontaneous ventilation is maintained.
The technique also has advantages over gaseous induction. First, low-dose propofol
provides excellent anxiolysis that notably assists the progress of anesthesia. Second,
increasing depth of anesthesia is independent of the patient's ventilation. This allows
rate of increase of the depth of anesthesia to be titrated carefully, by the anesthetist
(rather than dictated by the patient). It also means that if difficulty is encountered
stopping the infusion immediately enables anesthesia to lighten, without requiring the
patient to “blow off” anesthesia via an airway that was partly obstructed and has now
worsened. Finally, airway reflexes are rapidly obtunded, so coughing increased
secretions and the complications these lead to during gaseous induction are rare. In
many cases, patients will tolerate gentle manual ventilation even when still responsive
to verbal stimulus. This enables confirmation of ability to ventilate, or of increasing
difficulty, and airway adjuncts (e.g. , Guedel airway) are tolerated considerably earlier
and better than during gaseous induction. Importantly, the technique does demand
scrupulous attention to technique to detect problems with the airway early.
Why Introduce the PLMA ™ over a Bougie?

The PLMA ™ is a device with a pedigree in management of the difficult airway.16,21If

there is one weakness in PLMA ™ performance, it is that insertion can be more difficult
than for other supraglottic airway devices: conventional insertion techniques enable a
first-time insertion rate with the PLMA ™ of 87%, (∼5% lower than that for the LMA-
Classic ™).21There is ample evidence that the use of a bougie aids first pass success
with the PLMA ™, increasing success close to 100% without any increase in
morbidity.9,10Therefore, in circumstances where I consider first time success to be
strongly desirable, I insert the PLMA ™ over a reusable Smith Portex gum elastic
bougie: the type of bougie is important to minimize the risk of esophageal trauma.15,21
Why the Aintree Intubation Catheter?
The AIC is perhaps the ideal tube to use to (a) intubate via a supraglottic airway and (b)
intubate narrow airways.22It has the smallest external diameter (a little less than 7.0
mm) of any endotracheal tube that will fit over a standard size fiberscope and its ID (4.6
mm) means that it does not “rattle around” during use, making impingement on the
glottis unusual. Its use via the LMA-Classic™ and PLMA ™ in difficult airway
management is reported in two series.3,23Once placed it enables oxygenation and
then, depending on circumstances, placement of a larger endotracheal tube (railroaded
over it), or a smaller one (by passing an airway exchange catheter through it, followed
by the smaller tube).
What Are My Rescue Plans and Plans for Management of Problems at

Extubation?
The small minor diameter of the trachea raises the significant possibility of difficulties
with ventilation or intubation. If ventilation becomes impossible at any stage after
induction or intubation with an AIC is not possible, my plan is “graceful withdrawal”
before considering another plan. Both are designed before any “bridges have been
burnt.” Certainly I would avoid aggressive attempts at passing an endotracheal tube,
risking tracheal edema.
In the event of loss of the airway, presumably with hypoxia, my emergency rescue
technique will be high-pressure source ventilation using a Manujet (VBM
Medizintechnik, Sulz, Germany): unlike other “injectors” the Manujet incorporates a
pressure-reducing mechanism so that the anesthesiologist may deliver only the
minimum driving pressure to ventilate the lungs (so reducing the risk, and extent, of any
barotraumas).24Ventilation would be via the Ravussin cannula, placed before induction
of anesthesia. Profound hypoxia and a peri-arrest situation is not an ideal time to place
a cricothyroid cannula. Peterson examined almost 200 cases of difficult airway
management which led to medicolegal claims25: 42% of cases ended with “Cannot
Intubate Cannot Ventilate” situation and in two-thirds of these cases a surgical airway
was obtained but was placed too late to avoid poor outcome. Needle cricothyroidotomy
and high-pressure source ventilation performed in these circumstances were each
associated with a high incidence of barotrauma. Although these cases are undoubtedly
affected by outcome bias, the message is clear: waiting for Cannot Intubate Cannot
Ventilate situation and a peri-arrest patient before intervention is a poor plan. The
technique of insertion of a prophylactic cricothyroid cannula for difficult airway
management has been previously described26and is a frequent component of my
management of patients with airway obstruction. It is easily performed in the awake
patient, is almost painless, and is well tolerated. Ideally, the catheter would be placed
under fiberscopic control as this improves position and reduces complications27but in
this case that may not be practical. It is remarkable how much more confident one feels
when the rescue route is established before undertaking other difficult techniques that
may fail. Should I need to use the cricothyroid cannula I would not anticipate great
difficulty with inspiration but great care would be needed to ensure that full exhalation
had occurred (perhaps over 5-10 s or longer) before commencing the next breath:
placing a hand on the patient's chest and palpating complete chest fall is a useful
technique. Failure to confirm complete expiration would rapidly lead to severe
barotraumas.28
Knowledge Gap
For some questions in clinical anesthesia, there may be no correct answer or

alternatively several appropriate answers. The airway experts chose different airway
management strategies for this patient. Importantly, this does not support thoughtless
airway management: through this case scenario, one of the notable findings is that we
all fundamentally agreed that ventilation would be possible during anesthesia induction.
Despite this, why did we each choose different airway management strategies and
include in these plans backups in case of failure? Probably, this is either because
preoperative assessments of airway size and collapsibility may be imperfect in
predicting ease of ventilation during general anesthesia or because the airway
management techniques and devices currently available for managing tracheal stenosis
is also imperfect.
Critical Stenosis for Breathing and Mechanical Ventilation during General

Anesthesia
Even in patients with severe tracheal stenosis, normal gas exchange is maintained by
respiratory compensatory mechanisms. Therefore, the presence of hypercapnia in
preoperative patients without other respiratory diseases strongly indicates the potential
for failure of both spontaneous and mechanical ventilation during general anesthesia. In
contrast, the ability to compensate breathing through a narrow airway is well marked
during general anesthesia and sometimes better than that during wakefulness, because
behavioral influences such as panic and anxiety are eliminated and oxygen
consumption is reduced.29Nunn and Ezi-Ashi29found breathing through a tubular
resistor of 4.5 mm ID and 2.5 cm in length or 3.0 mm ID and 2.5 cm in length reduced
the mean minute ventilation by 7 and 21%, respectively, during general anesthesia,
although responses were variable and unpredictable. The subsequent studies by
Moote et al. (inspiratory resistive loads), Kochi and Nishino (inspiratory resistive loads),
and Isono et al. (expiratory resistive loads) confirm that the critical fixed narrowing
through which anesthetized patients can spontaneously breathe without an increase in
Paco2is 4.0-4.5 mm ID.30–32Respiratory compensation for breathing through a tubular
resistor is achieved by decreasing the respiratory rate, with prolongation of both
inspiratory and expiratory times and the increase in respiratory drive. Although the
patient's respiratory drive decreases or ceases during assisted and controlled
ventilation, tolerable size of the stenosis for breathing may not be greatly affected by the
ventilatory modes.2However, I found that no study has systematically examined the
critical stenosis for mechanical ventilation in anesthetized and paralyzed patients and
the speculation needs to be tested in the future.
Imaging Techniques for Assessment of Severity of Tracheal Stenosis
How can we assess structural and functional severity of tracheal stenosis? Patients with
mild to moderate tracheal stenosis rarely have clinical symptoms such as dyspnea.
Even patients with severe tracheal stenosis may present without stridor and dyspnea
during quiet breathing and, therefore, clinical symptoms may not be good indices for
severity of tracheal stenosis.33Various imaging techniques possibly assess the
structural severity of the stenosis. Chest radiographs have limited clinical utility for
determining the presence and the severity of an airway stenosis. Saggital CT images
along the airway provide significant information regarding the severity, location, and
shape of the airway narrowing and the structures surrounding the airway.34Recently
developed three-dimensional imaging techniques such as CT and magnetic resonance
imaging can more accurately delineate complicated airway shapes and determine the
minimal airway size.35Using a fiberoptic bronchoscope for measuring the cross-
sectional area and the length, the mean cross-sectional area and the length of stenotic
region of the trachea in patients who underwent trachea reconstruction surgery were
reported to be 48.3 ± 31.9 mm2(8 mm in diameter) and 9.3 ± 3.3 mm, respectively,
suggesting large structural variability among them.36Because of the structural variability
and complexity of the stenotic airway determined by the imaging techniques, functional
impact of the tracheal stenosis on breathing during general anesthesia is often difficult
to predict even by the sophisticated imaging techniques.
Potential Usefulness of Spirometry for Predicting the Obstruction Site and Airway
Collapsibility
Airway size is determined by the transluminal pressure across the airway wall and its
stiffness. A collapsible extrathoracic airway narrows during inspiration and dilates during
expiration because the transluminal pressure decreases during inspiration and
increases during expiration. In contrast, the relationship between airway caliber and
respiratory phase is opposite in the collapsible intrathoracic airway. Therefore, airflow
limitation predominantly (but not exclusively) occurs in the extrathoracic airway during
inspirations and in the intrathoracic airway during expiration.37,38This dynamic airway
behavior is exaggerated during forced expiratory and inspiratory maneuvers particularly
when collapsibility of the airway caliber is increased. In this context, old-fashioned
pulmonary function tests may be clinically useful for predicting the site of airway
occlusion and airway collapsibility.39,40Harrison39found that the mean PEF/PIF values
during a cycle of forced expiratory and inspiratory maneuvers were greater in 12
patients with extrathoracic airway obstructions than those of normal subjects (2.26 ±
0.84 vs. 1.32 ± 0.26). Two patients with collapsible intrathoracic tracheas had PEF/PIF
values less than 0.7, which increased to more than 1.0 after removal of the mediastinal
tumor and insertion of tracheal stent. In two patients with posttracheostomy tracheal
stenosis, both PEF and PIF were significantly decreased but PEF/PIF value did not
differ from normal subjects. According to the flow-volume loop in figure 1, our patient
had significant reduction in both PEF and PIF and a normal PEF/PIF ratio (1.33),
suggesting significant central airway stenosis and arguably adding evidence for rigidity
of the airway wall. Nevertheless, caution is required for interpretation of the results,
because PIF can be influenced greatly by patient effort.
Shamberger et al. 40demonstrated a direct association between the tracheal cross-
sectional area measured by the CT scan and PEF values in children with anterior
mediastinal tumors. Interestingly, they found significant but variable PEF reduction (2-
42% reduction) in the supine position compared with the sitting position and significant
PEF improvement in all children after therapeutic mass reduction. Azizkhan et
al. 41reported complete airway obstruction after induction of anesthesia in children with
greater than 50% tracheal narrowing. As these authors suggested, the patient with a
highly collapsible trachea (suggested by lower PEF and narrower tracheal cross-
sectional area) should not have general anesthesia induced before securing the airway.
In summary, spirometric variables may be useful for functionally characterizing tracheal
collapsibility and for detecting the risk of critical airway collapse after induction of
anesthesia, but further investigations are necessary.
Spirometry for Predicting Functional Airway Size for Breathing during General
Anesthesia
When the airway is rigid, the severity of airflow limitation is determined by airway size.
Among the spirometric variables, Empey33clearly demonstrated a significant
association between FEV1/PEF and the cross-sectional area of the central airway
stenosis, and therefore FEV1/PEF might be used as a clinically useful parameter for
predicting functional airway size without sophisticated imaging analysis. Because of the
complexity of the contribution of stenotic length and airway shape to total airway
resistance, FEV1/PEF may have advantages over imaging information as an index for
total upper airway resistance. Empey found that FEV 1/PEF ([ml · s−1]·[l · min−1]−1) was
greater than 10 in all patients with upper airway obstruction: equivalent to a normal
subject breathing through an external resistance of less than 6 mm diameter (fig. 4).
Breathing through a 4-mm orifice, possibly resulting in impossible mechanical ventilation
during general anesthesia, increased the FEV 1/PEF to more than 15. In our patient with
3 cm tracheal stenosis with minimal cross-sectional area of 59 mm 2, FEV1/PEF is
calculated as 1950/180 = 10.8. The FEV 1/PEF is much higher than that in normal
subjects and corresponds to breathing through a, at least, 6 to 8 mm orifice. Therefore,
this assessment suggests possible breathing or mechanical ventilation during general
anesthesia, assuming noncollapsible airway characteristics. This functional assessment
of the tracheal stenosis can give anesthesiologists significant information for
determining perioperative airway management strategies (fig. 1). An FEV 1/PEF of more
than 15 (equivalent to 4 mm orifice breathing) may indicate a potential inability of
mechanical ventilation after induction of general anesthesia, although this needs to be
validated and other approaches should be considered in future studies.
Fig. 4. (A ) Forced expiratory volume in the

first second/peak expiratory flow (FEV1/PEF)
in normal subjects with and without
resistances added at mouthpieces. Diameter
of orifice is shown in each case. (B )
FEV1/PEF in patients with lower airways
obstruction, interstitial lung disease, and
upper airways obstruction. Black circles
indicate cases requiring tracheostomy. PEFR
= peak expiratory flow rate. Reproduced and
modified from the BMJ, Empey DW, volume
3, pages 503-5, 1972, with permission from
BMJ Publishing Group Ltd.33
In conclusion, we discussed anesthetic management of a patient with tracheal stenosis

and found significantly different airway management strategies among us. Lack of
reliable and accurate prediction of airway patency and breathing during general
anesthesia in the patient with tracheal stenosis seems to be the fundamental reason for
the variable airway management strategies. For patients with difficult airways, our
progress in preoperative airway assessment as a predictive tool is rather limited, when
compared with the outstanding developments in airway management techniques and
devices.
Dr. Cook acknowledges Dominic Hurford, M.B.Ch.B., F.R.C.A., Special Registrar, Royal
United Hospital, Combe Park, Bath, United Kingdom, and Andy Giorgiou, B.Sc.,
M.B.Ch.B., F.R.C.A., Special Registrar, Royal United Hospital, with whom informal
discussion of the case assisted in clarification of concepts and details. Dr. Isono thanks
Toshihito Sai, M.D., Head of the Department of Anesthesiology, Naruto General
Hospital, Sanmu, Japan, for his assistance with preparation of this manuscript.
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Case Study: Typical Bilateral Femoral Fracture: Camarines Sur Polytechnic Colleges

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Republic of the Philippines

CAMARINES SUR POLYTECHNIC COLLEGES

Case Study: Typical Bilateral Femoral Fracture

risk for atypical femoral fractures is 1,78/100.000 person-years in patients receiving

A 75-year-old patient was transferred with an ambulance to our hospital because of

Patient’s medical history comprises hypertension, carotid stenosis, dyslipidemia,

Blood tests results: Ca=9.2mg/dl(8.4-10.2), P=3.9mg/dl(2.5-5.0), ALP=44U/L(40-150),

Figure 2. Bone scan

Figure 3. Bone scan

Figure 5. AP radiograph of both femoral shafts 1-year after surgery

simultaneously), hypertrophy or increased thickness of the cortex at the radiographs in

5. Nguyen ND, Eisman JA, Nguyen TV (2006) Anti-hip fracture efficacy of

6. Boonen S, Kay R, Cooper C, Haentjens P, Vanderschueren D, et al. (2009) Osteoporosis

7. Capeci CM, Tejwani NC (2009) Bilateral low-energy simultaneous or sequential femoral

15.Shane E, Burr D, Ebeling P, Abrahamsen B, Adler RA, et al. (2010) Atypical

16.Zafeiris CP, Stathopoulos IP, Kourkoumelis G, Gkikas E, Lyritis GP (2012) Simultaneous

20.Schilcher J, Michaëlsson K, Aspenberg P (2011) Bisphosphonate use and atypical

23.Gedmintas L, Solomon DH, Kim SC (2013) Bisphosphonates and risk of subtrochanteric,

26.Chiang CY, Zebaze RM, Ghasem-Zadeh A, Iuliano-Burns S, Hardidge A, et al. (2013)

27.Tarazona-Santabalbina FJ, Aquilella-Fernadez L (2013) Bisphosphonate long-term

28.Çakmak S, Mahirogullari M, Keklikçi K, Sari E, Erdik B, et al. (2013) Bilateral low-energy

29.Ovaska MT, Makinen TJ, Madanat R (2011) Simultaneous bilateral subtrochanteric

31.Tarun Pankaj J, Murray T (2012) Atypical femoral fractures related to bisphosphonate

Case Study: Haemorrhagic shock following

A contrast-enhanced CT scan revealing multiple regions of contrast extravasation in the

Retroperitoneal haematoma associated with fractures of the transverse processes of

Outcome and follow-up

As for treatment, transcatheter arterial embolisation of the affected vessels is effective

Case Study: Methanol Poisoning in a Child

Diagnosis of methanol poisoning is based on the suspicion of ingestion, the presence of

In the liver, methanol is removed by biotransformation via alcohol dehydrogenase

That methanol by itself is not toxic. It is the degradation of methanol by alcohol

Case Study: Burns

 3-year old boy, presents to pediatric ED with mother

 Wrapped child’s hands in towels and brought to ED

 No other injuries noted

 PMHx: Had orchidopexy for an undescended testicle at 15 months of age,

 Allergies: Penicillin – Rash

 Glucose: Not Done

 H+N: Normal, no obvious burns or singe to oropharynx or nares

 Cardiac: N S1S2, no murmurs noted

 Resp: AE=AE, no wheeze, no stridor, no obvious increased work of breathing

 Abdo: Soft, non tender with N bowel sounds

 Hands look as follows……

 CR: 1-2 seconds in all digits

 Still moving all fingers and wrists

 Mom able to convince child to give a thumbs up

 Child’s hands covered in ointment containing

 Wrapped in gauze, mother advised to change daily with

 daily application of ointment

 Given follow up appointment with plastics because of

 Child happy and eating popsicle on way out of the

 Relatively common injuries caused by direct or indirect

 contact with heat, electrical current, radiation, or

 With thermal burns, the severity of injury is dependent

 on length of exposure, the temp, and the intrinsic

 tissue structure leading to heat conductivity

 Common denominator in burn injuries is protein

 denaturation and cell death (either by necrosis or

 Temperatures below 440 C are generally tolerated without injury. However, as

 Traditionally burns are separated into 3 concentric zones: Coagulation,

 The cont’d progression of burn injuries is multifactorial and not completely

 There is an occlusion of the dermal microcirculation with a combination of red