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Fall 2019

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Fall 2019

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© © All Rights Reserved
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Volume X I I I Issu e I

Emergency Medicine

Annals of B Pod

fall Issue 2019


S i n c e 1 9 7 0 - L e a d e r s h i p - E x c e l l e n c e - O p p o r t u n i t y
+
Air Care:Hypokalemia
Annals of B Pod

K
Fall 2019

Adam Gottula, MD
2 Hypokalemia Gottula
University of Cincinnati R3
4 Malaria Laurence
6 Traumatic Diaphragmatic Rupture
Laurence
History of Present Illness
8 Acute Pancreatitis Frederick
Air Care was dispatched to a referring hospital for a middle aged female who presented
Back EKG Focus: Hypokalemia Scanlon with lower extremity weakness. Upon presentation to the hospital, the patient was som-
Cover nolent with weakness in the bilateral lower extremities and full strength in her upper ex-
tremities. Providers were concerned for stroke. The patient underwent a non-contrast CT
scan and prior to any therapeutic interventions suffered a pulseless electrical activity (PEA)
arrest. The patient received chest compressions and two rounds of epinephrine with return
of spontaneous circulation (ROSC) after 6 minutes. The patient was intubated and started
on an amiodarone drip following a brief episode of wide complex tachycardia. Following
ROSC the patient’s labs resulted with a potassium of 1.5 mEq/L. 10 mEq of potassium
chloride was started via a peripheral line.

Past Medical History Medications


Bipolar disorder, morbid obesity,
hypertension, hyperlipidiemia, Unknown
COPD
Allergies
Past Surgical History Unknown
Unknown

Physical Exam
HR BP RR SpO2
Editors 88 90/60 24 84% ventilator
Michael Klaszky, MD Volume Assist Control: RR 16, TV 550cc , PEEP 8, FiO2 100%
Matthew Scanlon, MD
David Habib, MD The patient was pale, obese, and ill appearing on the ventilator. Breath sounds were sym-
Simanjit Mand, MD metric. Patient was in normal sinus rhythm on the monitor, with occasional premature
James Makinen, MD ventricular complexes (PVCs). The patient’s pupils were equal, round and reactive to light
(4-->2mm). She opened her eyes and moved all four extremities to command.
Adam Gottula, MD
Meaghan Frederick, MD Pre-Hospital Interventions
Colleen Laurence, MD Upon HEMS arrival, the first 10 mEq of potassium had completed administration. An ad-
Emily Roblee, MD ditional 10 mEq of potassium was ordered and administered prior to departure. Imme-
diately after takeoff, the patient became bradycardic to the 20s and pulseless. The patient
underwent resuscitation via ACLS guidelines, and ROSC was achieved after 8 minutes.
Faculty Editors
William Knight, MD The patient remained hypotensive with a normal sinus rhythm and frequent PVCs. The
Natalie Kreitzer, MD remaining potassium was rapidly administered intravenous push with resolution of the pa-
tient’s PVCs. 20 ug of epinephrine was administered with improvement in blood pressure
Robbie Paulsen, MD to 100/60. The patient remained stable throughout the rest of the flight. At the receiving
Ryan LaFollette, MD tertiary care center the patient’s initial blood gas was significant for a normal pH and po-
Kari Gorder, MD tassium of 1.7 mEq/L.
Grace Lagasse, MD
Jessica Baez, MD Discussion
Potassium was first isolated from potash by Sir Humphrey Davy in 1807, but the biologic
significance of potassium was not recognized until over one hundred years later. Potassium
Founding Editors is primarily an intracellular cation, with concentrations 30- 40-fold greater intracellularly
Aaron Bernard, MD than extracellularly. This differential is achieved by the sodium-potassium ATPase enzyme
Christopher Miller, MD found in the plasma membrane of cells. ATPase hydrolyzes ATP to pump three sodium
ions out of the cell in exchange for two extracellular potassium ions into the cell. This gra-
dient facilitates an outward current of potassium through potassium-selective ion channels

2 Annals of B Pod
in the plasma membrane resulting in a negative resting membrane on EKG. Initial changes include T wave flattening/inversion, PR
potential (RMP) in the cardiac myocyte. The negative RMP works prolongation, prominent U waves, and ST depression. The U wave
to stabilize excitable tissue, such as atrial and ventricular myocytes, is a small (0.5 mm) deflection immediately following and in the
thus preventing spontaneous action potentials. With hypokalemia, same direction as the T wave, best seen in V2 and V3.6 The later
the repolarization reserve is reduced. This leads to intracellular cardiac effects of hypokalemia include fatal arrhythmias such as
sodium and calcium accumulation leading to early afterdepolar- bradycardia, ventricular tachycardia, ventricular fibrillation, and
ization arrhythmias such as polymorphic ventricular tachycardia Torsades de Pointes. “Classic” ECG findings have poor sensitivity
(VT), which can degenerate to ventricular fibrillation (VF) causing for diagnosing hypokalemia, as many patients with low potassium
sudden cardiac death. have a normal ECG.

Prior to initiation of treatment for hypokalemia it is first important


Causes of Hypokalemia to assess whether the patient has pseudohypokalemia. Pseudohy-
pokalemia is an aberrant laboratory phenomena where a sample
Abnormal Losses Transcellular Shift
from a patient with a normal potassium is reported as hypokale-
1) Medications 1) Medications
mic. This is a laboratory phenomenon caused by both delayed sam-
- Diuretics - Insulin
ple analysis and leukocytosis. When rechecked the potassium will
- Laxative/Enemas - Beta-2 sympathomimetics
usually be normal provided sample analysis is not again delayed. It
- Corticosteroids - Decongestants
is however important not to delay potassium administration in a
2) Gastrointestional losses - Xanthines
patient with a classic history and EKG changes while awaiting con-
3) Renal losses - Amphotericin B
firmation. Once the diagnosis of hypokalemia is certain further
- Osmotic diuresis - Verapamil
laboratory work-up must be pursued if a cause is not known. When
- Mineralocorticoid excess 2) Alkalosis
there is concern for renal losses of potassium, urine potassium and
- Type 1&2 renal tubular 3) Refeeding Syndrome
potassium-to-creatinine ratios should be checked.
acidosis 4) Increased beta-2 adrenergic
- Polydipsia stimulation
Initial treatment is focused on preventing cardiac conduction dis-
4) Hypomagnesemia - Delirium tremens
turbances and neuromuscular dysfunction by repleting potassium.
5) Dialysis - Head injury
Goal potassium levels are > 3.6 mEq/L for the general popula-
- Myocardial ischemia
tion and > 4.0 mEq/L for patients with a history of heart failure
5) Thyrotoxicosis
or myocardial infarction.6 Empiric administration of magnesium
Inadequate intake Pseudohypokalemia should be considered as patients will be unable to absorb potas-
1) Anorexia 1) Extreme leukocytosis sium in a hypomagnesemic state. This is a consequence of the ef-
2) Dementia 2) Delayed sample analysis fects of magnesium on the luminal potassium (ROMK) channels
3) Starvation within the connecting tubule and cortical collecting tubules of the
4) Total parenteral nutrition kidney. Low levels of intracellular magnesium decrease the mag-
nesium-mediated inhibition of the ROMK channels leading to
Table 1 Causes of hypokalemia. increased renal potassium secretions, ultimately decreasing the ef-
ficacy of potassium replacement.7
Hypokalemia is defined as potassium less than 3.6 mEq/L (3.6
mmol/L) and is present in up to 21% of hospital-
ized patients and 2-3% of outpatients.1,2,3 The most
frequent causes of hypokalemia are diuretic use and Laboratory Analysis in Hypokalemia
gastrointestinal (GI) illness. Diuretic-induced hypo-
kalemia occurs through direct renal loss, is dose-de- - Repeat serum potassium measurement
pendent, and tends to be mild (3 - 3.5 mEq/L).4 The - Obtain serum glucose and magnesium levels
mechanism by which upper GI loss induces hypo- - Obtain urine electrolyte (24 hour timed urine potassium collection is the most accu-
kalemia is indirect and is thought to result from a rate) and creatinine levels
maladaptive renal response to the vomiting induced - Assess acid-base balance
alkalosis. Lower GI losses in the form of diarrhea - Consider thyroid and adrenal work-up if initial work-up is unrevealing
can also result in hypokalemia, as a portion of dai-
ly potassium is excreted in the colon. Hypokalemia Normal urine potassium excretion: 15 - 30 mEq/L
secondary to lower GI losses may be accompanied Spot Potassium-to-Creatinine ratio: < 1.5 mEq/mmol (> than 1.5 mEq/mmol is indicative
by hyperchloremic acidosis.5 Less common causes of renal potassium wasting)
of hypokalemia include renal tubular acidosis, tran-
scellular shift, and inadequate intake. Table 2 Laboratory analyses to consider in hypokalemia.

It is important to evaluate for possible GI losses, review medications Replacement of potassium is simple and formulaic. Serum po-
(diuretics, laxatives etc.), and assess for underlying cardiac comor- tassium concentration decreases approximately 0.3 mEq/L (0.3
bidities. Neurologic manifestations can range from generalized mmol/L) for every 100-mEq (100-mmol)
weakness to ascending paralysis, though the latter is uncommon- reduction in total body potassium.8 Us- Hypokalemia
ly seen. Early cardiac effects of hypokalemia can be demonstrated ing the patient’s measured potassium continued on page 12

Annals of B Pod 3
Colleen Laurence, MD MPH
Malaria follow-up with a primary care provider regarding his thrombocyto-
University of Cincinnati R2 penia.

History of Present Illness Visit 2


A male in his 30s first presents to the Emergency Department (ED) T 37.1 °C / HR 71 / BP 125/74 / RR: 18 / SpO2: 98%
with a chief complaint of headache three times over a five-day period. WBC 5.9 / Hgb 12.1 / Hct 35.9 / Plt 84
Onset of the headache was one week prior to presentation and has BMP / LDH / Haptoglobin / Fibrinogen / PTT / PT / INR / LFTs /
been intermittent since then. The patient describes the headache as ADAMST13 negative
throbbing and diffuse in nature, localizing it to his sinuses and tem- D-Dimer 2.82
poral area. Ibuprofen and combined acetaminophen-acetylsalicylic CT head non-con / CTA head negative
acid-caffeine tablets have provided some intermittent relief. The pa- LP opening pressure 31cm H2O / CSF studies negative
tient denies a history of chronic headaches and known sick contacts. ---
The patient does, however, note that he had recently received the in- The patient received symptomatic treatment with morphine,
fluenza vaccination. On review of systems, the patient endorses re- prochlorperazine, diphenhydramine, and two liters of intravenous
cent subjective fevers and chills as well as dark urine. He denies neck fluids with subsequent resolution of his headache. He was discharged
stiffness or pain, dizziness, gait disturbance, cough, congestion, sinus with recommendations for oral hydration and a prescription for oxy-
pain, photophobia, or preceding fall or trauma. The patient was born codone-acetaminophen.
in western Africa but had not traveled outside of the United States in
the past three years. He reports working at a “desk job” as he termed Visit 3
it, as a systems analyst with no environmental or chemical exposures. T 39.3 °C / HR 87 / BP 123/66 / RR 18 / SpO2 97%
WBC 6.0 / Hgb 11.5 / Hct 34.6 / Plt 75
Past Medical History: Typhoid fever BMP / Respiratory viral panel / HIV / LFTs / Acute hepatitis panel
Past Surgical History: Tooth extraction negative
Medications: None Thick and thin blood smears: Present, sug-
Allergies: Ampicillin gestive of Plasmodium ovale or Plasmodi-
um vivax, 0.6% parasitemia
Physical Exam ---
The patient was well appearing. He was alert The patient was admitted to medicine. Two
and oriented, moved all four extremities, and
had intact cranial nerves, sensation, and mo-
tor function throughout. He demonstrated no
signs of ataxia on finger-to-nose testing or in
his gait. He was able to range his neck fully and
demonstrated no meningismus with a negative
Brudzinski sign. His head was atraumatic. There
were no signs of scleral icterus. Conjunctiva Image 1: Thin smear. Courtesy of https://microbeonline.com/
were normal. There was no tenderness on pal- microscopic-diagnosis-of-malaria/
pation of his sinuses. His tympanic membranes
and oropharynx were clear without erythema or exudate. His lungs peripheral blood
were clear to auscultation bilaterally and the patient did not appear cultures as well as
in any distress. He had a regular rate and rhythm with no murmurs, labs to assess for
rubs, or gallops and 2+ radial pulses bilaterally. His abdomen was metabolic, autoim- Image 2 Thick smear . Courtesy of https://microbeonline.com/
microscopic-diagnosis-of-malaria/
soft, non-distended with no rebound or guarding. He had no signs of mune, and other
organomegaly with deep palpation. There was no obvious peripheral infectious etiologies were ordered. The Infectious Diseases (ID) ser-
edema or rash. vice was consulted. On hospital day two, his thick and thin peripher-
al blood smears returned positive for malarial organisms – thought
Visit 1 likely to be Plasmodium ovale or Plasmodium vivax given their mor-
T 39.6 °C / HR 94 / BP 135/84 / RR 17 / SpO2 98% phology and the patient’s history. The patient had a relatively low
WBC 4.9 / Hgb 13.5 / Hct 40.9 / Plt 103 parasitemia burden at 0.6%. Treatment with atovaquone-proguanil
BMP / Influenza / Mononucleosis / UA negative 1000-400 mg was initiated and subsequently completed on hospital
CXR negative day four. Patient discharged with ID follow up on hospital day five.
---
He was treated symptomatically with acetaminophen, ketorolac, Discussion
metoclopramide, diphenhydramine, and one liter of normal saline Febrile illness in patients who have lived or traveled abroad are often
with significant improvement in his headache. He was advised to attributable not to tropical disease but rather typical viral illnesses.

4 Annals of B Pod
Nonetheless, malaria and other tropical diseases should be consid- periods, and illness severities, which influence clinical presentation
ered in patients who have spent time in endemic regions. and antimalarial options.

Epidemiology Lifecycle of Malaria


Malaria is caused by protozoal parasites of the genus Plasmodium. Once the female Anopheles mosquito bites a human, thus transmit-
There are five Plasmodium species that are known to cause disease ting the Plasmodium, the sporozoite form of the parasite travels first
in humans: falciparum, vivax, malariae, ovale, and knowlesi. While to the liver where they infect liver cells and undergo asexual repro-
global efforts to prevent the spread of malaria have reduced mortality duction. They produce merozoites that rupture from the infected cells
from malaria by an estimated 25% between 2010 and 2016, Plasmo- and are released into the blood stream. This process is termed the
dium species remain a major cause of morbidity within the global exoerytherocytic stage. Importantly and as we saw in our patient, the
community.1 In 2017, the World Health Organization (WHO) es- P. vivax and P. ovale may also enter a dormant stage at this time with
timated 219 million cases of malaria in 90 countries and recorded a form of the parasite called a hypnozoite persisting in the liver until
435,000 deaths due to malaria. Sub-Saharan Africa (SSA) carried a weeks, months, or even years later, when they are released into the
disproportionate share of the global malaria burden, with 92% of ma- blood stream. More often, however, merozoites then invade erythro-
laria cases and 93% of deaths attributable to malaria in 2017. Howev- cytes, asexually multiply to produce more daughter merozoites, and
er, India, along with Nigeria, the Democratic Republic of the Congo, release them into the blood stream to perpetuate reproduction, de-
Mozambique, and Uganda, accounted for nearly half of all malaria stroying the erythrocyte and causing hemolysis in the process. This
cases worldwide that occurs during the eryth-
year.2 rocytic stage and is when
most patients develop
The majority of malaria symptoms of malaria.
infections in the United
States occur in individ- At this time, some of the
uals who have traveled parasites may also differ-
to areas with ongoing entiate into sexual repro-
malaria transmission. In duction to produce male
2015, 1,517 confirmed (microgametocyte) and
cases of malaria in the female (macrogameto-
U.S. were reported to the cyte) gametocytes, which
CDC. P. falciparum, P. are released into the blood
vivax, P. ovale, and P. ma- stream and taken up by
lariae were identified in the mosquito during their
67.4%, 11.7%, 4.1%, and next blood meal. In the
3.1% of cases respective- mosquito, the sporogenic
ly, and the species was cycle commences. The mi-
not reported or was in- crogametocyte penetrates
determinate in 12.9% of the macrogametocyte to
cases. 17.1% of the cases produce a zygote, which
were classified as severe develops into a motile
illness, and 11 persons Figure 1: Life cycle of malarial parasite. Courtesy of https://commons.wikimedia.org/wiki/File:Malaria_lifecycle-CDC.gif ookinete that invades the
died as a result of infec- gut wall and develops into
tion in 2015.3 an oocyst. Eventually, these oocysts rupture, releasing sporozoites,
which travel to the mosquitos’ salivary glands and perpetuates malar-
The persistence of malaria in certain regions of the world stems from ia’s life cycle when they, in turn, invade their next human host.8 No-
a complex interplay of multiple factors, including limited resources tably, malaria may also be transmitted by blood transfusion or passed
and socio-economic instability which complicate malaria control. transplacentally from mother to fetus, though this is rare.
These issues are further compounded by the tropical and subtropi-
cal geography and climate that facilitates year-round transmission by Clinical Presentation
malaria’s vector, the female Anopheles mosquito. Certain Plasmodi- The clinical manifestations of malaria vary with species, immune
um species variably predominate in different regions: P. falciparum status, and age of the human host, among other factors. Individuals
has the broadest reach, accounting for the majority of cases in SSA, are generally asymptomatic until the parasites reach the erythrocytic
southeast Asia, the Eastern Mediterranean, and the Western Pacific.4 stage. The incubation period following the bite of an infected Anoph-
Conversely, P. vivax is more common in the Americas, representing eles mosquito ranges from one to four weeks. Longer incubation pe-
74.1% of the cases.5 P. malariae and P. ovale are both rarer in gen- riods are more common in semi-immune individuals and in those
eral and occur most often in SSA, though P. malariae is found in all on chemoprophylaxis. Infection with P. falciparum typically becomes
endemic areas.6 Finally, P. knowlesi has been identified in southeast clinically apparent within seven to fourteen days, with virtually all
Asia and, as yet, is still considered a zoonotic species, as it has not infected hosts demonstrating symptoms within one month following
been known to pass from human to human without an intermediate inoculation. By contrast, vivax, malariae, and
host, the macaque monkey.7 The species of malaria is important to ovale infections commonly have longer incuba- Malaria
consider as the species have slightly different life cycles, incubation tion periods, ranging anywhere from fourteen continued on page 14

Annals of B Pod 5
Traumatic Diaphragmatic
Rupture
Colleen Laurence, MD
University of Cincinnati R2
History of Present Illness
The patient is an otherwise healthy middle aged female who
presents following a motor vehicle collision. She is the re-
strained driver of a vehicle with significant front end damage,
air bag deployment, and prolonged extrication. On arrival of
helicopter emergency services (HEMS), the patient was hypo-
tensive to 40/30s, tachycardic to 140, had an oxygen saturation
in the 80s, and a GCS of 4 (1/1/2). She was intubated via rapid
sequence induction with ketamine and succinylcholine, and she
received 2 units of fresh frozen plasma (FFP), 1 unit of packed
red blood cells (pRBCs), and 1 gram of tranexamic acid (TXA).
HEMS providers also noted decreased breath sounds in the left
lung field and performed needle decompression on the left in
the midaxillary line with reported improvement of her hypoxia.

Physical Exam
HR BP RR SpO2
128 159/126 27 100% ventilator

General: Intubated. Immobilized on backboard with a cervical


collar.
Image 3: Representative chest X-ray dpicting left-sided diaphragmatic rupture with herniation of
HEENT: Left forehead laceration, pupils 4-5 mm bilaterally. abdominal contents
Neck: Trachea midline
Pulmonary: Clear to auscultation bilaterally with no wheezes or
Pelvis: Left pubic fracture
crackles. No chest wall crepitus. Needle decompression catheter
CT Head – left frontal and temporal contusions/shear
present in the mid-axillary line.
CT Chest: Left diaphragmatic rupture, traumatic aortic injury
Abdomen: Soft, non-distended. No tenderness to palpation. No
with pseudoaneurysm, multiple pulmonary lacerations, bilater-
masses appreciated. No external evidence of trauma. Pelvis sta-
al pneumothoraces left greater than right, right 1st rib fracture,
ble to compression with T-pod in place.
left 2-4, 6-9 rib fractures
Musculoskeletal: Lacerations to bilateral lower extremities dis-
tal to the knees. Left foot externally rotated and shortened with
open left ankle fracture. No step-offs or deformities of the cer-
vical, thoracic, or lumbar spine. Normal rectal tone.
Skin: Cool, pale
Neurologic: Intubated. GCS 1,T,4

Diagnostic Work Up
10.7
24.8 260 143 108 13 213
31.7 3.5 25 1.37

Lactate: 4.0
pH 7.2 / pCO2 57 / base deficit: 6.3

TEG ACT: 128 / R time: 50 / Time: 75 / Angle: 76.2 / Max Am-


plitude 66.1 / Lysis 30: 1.1 Image 4: Representative CT chest depicting left-sided diaphragmatic rupture with herniation of
abdominal contents

6 Annals of B Pod
Hospital Course as well.2
The patient is assessed and managed in collaboration with the
Diaphragm Injury Scale
trauma team. The patient has a GCS of 5T (1-T-4) on arriv- Given the high-
Grade Description of Injury er-impact mech-
al. She ultimately receives an additional 2 units of packed red
blood cells (pRBC)and 1 unit of fresh frozen plasma (FFP) for I Contusion anisms that are
a total of 4 units of pRBCS and 3 units of FFP. Once stabilized, associated with
II Laceration <2cm traumatic dia-
she undergoes additional imaging. She is then taken to the op-
phragmatic rup-
erating room where she undergoes an exploratory laparotomy, III Laceration 2-10cm ture, it is not
splenectomy, simple hepatorrhaphy, and reduction of her stom-
ach, spleen, and colon from the thoracic cavity and repair of the IV Laceration >10cm with tissue loss surprising that ap-
diaphragmatic defect. The left chest is irrigated, and a left chest ≤25cm 2 proximately 50%
tube is placed. She is discharged on hospital day 26 and contin- of patients with di-
V Laceration with tissue loss > 25cm2 aphragmatic injury
ues to improve with rehabilitation and follow up with specialists
for her multiple injuries. suffer concomitant
Advance one grade for bilateral injuries up to grade III
injuries.9,10 Among
patients found to
Discussion Table 3: Diaphragm Injury Scale depicting grades of diaphrag-
have traumatic di-
matic injury
Diaphragmatic injury is relatively uncommon, comprising less aphragmatic rup-
than 1% of all traumatic injuries.1,2 Diaphragmatic rupture typ- ture, 48% have liver injuries, 47% have a hemothorax and/or
ically occurs in association with other thoracic and abdominal pneumothorax, 35% have splenic injuries, 28% have rib frac-
organ injuries. It may result from both penetrating trauma and tures, 23% have bowel injury, 16% have kidney injuries, 14%
blunt trauma, though there is a higher incidence of traumatic have pelvic fractures, 11% have closed head injuries, 4% have
penetrating diaphragmatic injury (67%) compared to traumatic thoracic aorta injuries, and 4% have spinal cord injuries.2
blunt diaphragmatic injury (33%).3
The difficulty in diagnosing diaphragmatic trauma is twofold:
In blunt trauma, rupture is thought to occur due to an abrupt the first being that patients often present with polytrauma, and
increase in the intraabdominal pressure. At baseline, there is a more apparent injuries at the time of initial evaluation tend to
positive pressure gradient of 7-20 cm H2O between intraperi- take precedence. In conjunction with this, there is no particular
toneal and intrapleural pressures, which can increase ten fold physical exam finding that is pathognomonic for a diaphrag-
with severe abdominal trauma. This pressure overcomes the matic rupture. Patients are often asymptomatic initially and
strength of the diaphragmatic tissue, avulsing or shearing the may only become significantly symptomatic in later stages of
diaphragm from its various attachments.4,5,6 Blunt trauma most the injury course.
often causes large radial tears in the diaphragm; by comparison,
penetrating trauma typically causes smaller defects in the dia- Complications from diaphragm rupture include not only the
phragm, primarily where the intrusive object has directly dam- herniation of bowel contents into the limited space of the chest
aged this structure. Thus, penetrating diaphragmatic injuries wall leading to displacement of lung tissue and other intra-tho-
are more likely to be missed because of their smaller size.3 racic contents, but also elimination of one of the primary respi-
ratory muscles that assists with oxygenation and ventilation. Di-
The left posterolateral hemidiaphragm is most commonly in- aphragmatic injury affects respiratory status significantly, and if
jured due to the relative weakness of the left hemidiaphragm, the injury is severe enough or goes undetected for long periods
whereas the right hemidiaphragm is protected by the liver. In of time, patients may develop tachypnea, hypoxia, tachycardia,
one review of 1589 patients, left-sided injury was noted in 75% and hypotension. The other consideration in this injury is to
of the cases, right-sided injury in 23%, and bilateral injuries in the bowel itself, which can progress quickly to bowel strangula-
2%.7 In additional to laterality, the severity of the defect should tion, ischemic gut, and multiorgan failure. Thus, without early
also be considered. The American Association for the Surgery detection and intervention, diaphragmatic defects tend to grow
of Trauma (AAST) classifies diaphragm injuries using the or- over time with escalating consequences on patient morbidity
gan injury scale (Table 3). If bilateral diaphragmatic injuries and mortality.
are present, the injury grade is automatically a Grade III. It is
important to note, however, that this scale has yet to be studied The second difficulty in diagnosing diaphragmatic injury is that
for its correlation with morbidity and mortality and does not the most common imaging modalities used in the initial evalu-
determine specific management.8 ation of trauma patients do not have the desired level of accu-
racy in detecting early trauma. Chest radiography is a common
Diagnosis initial imaging modality for most trauma patients and may re-
The diagnosis can be challenging to make, so a high index of veal elevation or blurring of the hemidiaphragm, hemothorax,
suspicion is paramount. Evaluation for diaphragmatic injury or abnormal gas patterns obscuring the hemidiaphragm that
begins with the patient history and identification of the injury may indicate underlying trauma. However, chest radiography
mechanism, physical exam, and assessment of associated inju- is not sensitive and can appear normal 50% of the time when a
ries. Motor vehicle collisions are responsible for up to 90% of true diaphragm injury exists. One study
blunt diaphragm ruptures, but a high level of suspicion should attributed a sensitivity of 46% to chest Traumatic Rupture
be maintained in patients presenting with fall or crush injuries radiographs in detecting left-sided rup- continued on page 13

Annals of B Pod 7
Acute Pancreatitis
Meaghan Frederick, MD
University of Cincinnati R2
History of Present Illness
A middle aged male with a past medical history of hypertension,
cholecystectomy, and a previous episode of pancreatitis presents
to the ED with one day of constant epigastric abdominal pain ra-
diating to the back with associated bloating. He denies any fevers,
nausea, vomiting, or diarrhea. The patient denies prior abdominal
surgeries or instrumentation with the exception of a prior chole-
cystectomy. He endorses alcohol and marijuana use. The patient
is mildly hypertensive and tachycardic with a taut, diffusely ten-
der abdomen and voluntary guarding. His blood work is notable
for a mild leukocytosis of 12.9 with otherwise unremarkable renal
panel, hepatic function testing, and lipase. A CT abdomen/pel-
vis demonstrates a 10 cm x 9 cm peripancreatic fluid collection
suggestive of pseudocyst formation, with narrowing of the portal Image 4: Representative ultrasound depicting FAST exam
vein and splenic vein occlusion. The patient’s pain improves with
symptomatic treatment. Gastroenterology is consulted and the pa-
tient is planned for outpatient esophagogastroduodenoscopy and
discharged home.

The patient returns to the ED the next day with significant wors-
ening of epigastric abdominal pain unmitigated by his home oral
pain medication.

Past Medical History


Pancreatitis in 11/2018 Medications
Hypertension Amlodipine, lisinopril,
pantoprazole, oxycodone
Past Surgical History
Cholecystectomy Allergies
Ciprofloxacin
Social History
Alcohol, marijuana

Image 5: Representative CT abdomen/pelvis depicting unchanged walled-off peripancreatic fluid


Physical Exam collection compared to the prior study. Stable portal vein thrombosis with significant interval wors-
ening of ascites concerning for significant flow impedance. There is also mild wall thickening and
Temp HR BP RR SpO2 fat stranding about the transverse and proximal descending colon which is likely due to portal vein
36.4 117 185/102 19 97% on RA thrombus resulting in increased venous pressure.

Lying in bed, uncomfortable and diaphoretic. He is tachycardic


with a regular rhythm. Normal respiratory effort with relative- Hospital Course
ly shallow breaths secondary to abdominal pain. His abdomen is The patient was admitted to acute care surgery. He was placed on
diffusely tender, distended, with guarding and rebound as well as a heparin drip to treat his portal vein thrombosis and was gradu-
moderate rigidity. ally transitioned to enoxaparin. The patient began to have nausea,
vomiting, and constipation with concern for secondary small bow-
Diagnostic Work Up el obstruction for which a nasogastric tube was placed. Gastroen-
terology was consulted and, after reviewing the patient’s images,
15.1 suggested that the peripancreatic fluid collection was more con-
20.8 250 134 94 12 162 sistent with walled-off necrosis than a pancreatic pseudocyst. The
46.1 3.7 29 0.98 patient subsequently underwent cystogastrostomy with drainage
of 500 mL of fluid and debris. The nasogastric tube was removed,
AST 15 / ALT 10 / ALP 64 / TBili 0.8 / DBili 0.3 / Lipase 75 his constipation resolved, and the patient was able to tolerate oral
intake. He was discharged home on enoxaparin with plans for re-
peat imaging in the following weeks.

8 Annals of B Pod
Discussion without objective evidence of organ dysfunction. These patients are
Etiology and Disease Severity most often managed conservatively and may be discharged safely
Acute pancreatitis is defined as a serum lipase at least three times with overall low morbidity and mortality. Moderately severe pan-
the upper limit normal, abdominal pain consistent with acute pan- creatitis is characterized by either transient organ failure or local
creatitis (acute, severe, epigastric pain often radiating to the back), or systemic complications in the absence of persistent organ fail-
and findings consistent with acute pancreatitis on CT, MRI, or US ure (>48 hours). Outcomes of moderately severe acute pancreatitis
imaging. The presence of two out of the three criteria is considered vary drastically, ranging from complete recovery to death, though
diagnostic. Acute pancreatitis can further be classified by morphol- the associated mortality remains significantly lower than that of se-
ogy and severity. vere acute pancreatitis. Severe pancreatitis is defined as persistent
organ failure lasting beyond 48 hours and is thought to affect 20-
Morphologically, there are two categories of pancreatitis: acute 30% of all patients suffering from acute pancreatitis.9 Severe pan-
edematous interstitial pancreatitis and acute necrotizing pancre- creatitis carries a mortality rate as high as 50%, and potentially be
atitis. Interstitial edematous pancreatitis is the most common pre- even higher when complicated by pancreatic necrosis.14
sentation, defined by diffuse inflammatory edema of the pancreas
on imaging. Necrotizing pancreatitis, by comparison, is relatively Epidemiology
rare, occurring in <10% of patients with acute pancreatitis. It most Acute pancreatitis has an estimated incidence of 13 to 45 cases per
commonly manifests as necrosis of both the pancreas and peripan- 100,000 individuals and carries a mortality of approximately 5%
creatic tissues, rarely damaging either structure in isolation. Ra- for all patients. Gallstones are the most common cause of acute
diographic findings typically develop on CT imaging over several pancreatitis, accounting for approximately 35-40% of all causes. In
days. This necrotic tissue is at high risk of superimposed infection, the United States, alcohol use is implicated in roughly 30% of cases
potentially leading to additional complications discussed in great- of acute pancreatitis, making it the second most prevalent etiology
er detail below. Prognostication and identification of high-risk pa- of pancreatic injury. Beyond gallstones and alcohol use, episodes
tients are confounded by the lack of correlation between the extent of pancreatitis may stem from pathologic anatomic variants such
of necrosis and likelihood of it becoming infected in addition to as pancreatic divisum, infectious agents, toxicologic exposures,
the delayed nature of infections, with most occurring greater than hypercalcemia, hypertriglyceridemia, hypothermia, mumps, cock-
one week following the insult. A necrotizing infection is defined sackie A virus, HIV, tuberculosis, and the rare but memorable scor-
radiographically by extra-luminal gas in the pancreas or peripan- pion sting.26
creatic tissues on CT. It is important to recognize pancreatic ne-
crosis as it often necessitates the use of antibiotics in addition to Treatment
traditional therapies. Fluid Resuscitation
Patients with acute pancreatitis are prone to hypovolemia due to
The severity of acute pancreatitis is divided into mild, moderate, and decreased oral intake and third spacing. This hypovolemia can
severe. Mild acute pancreatitis is defined by features of pancreatitis worsen outcomes by predisposing patients to renal injury and
cardiovascular collapse, as well as increasing the risk of perfusion
defects to the already damaged pancreas. There are numerous
Acute Pancreatitis guidelines with varying recommendations regarding the appro-
Definition (2 out of 3 criteria): priate volume for intravascular repletion, rate of resuscitation, and
Lipase >/= 3X upper limit of normal choice of crystalloid agent. Of the available crystalloid products,
Abdominal pain Lactated Ringers (LR) confers the theoretical benefits of decreasing
Diagnostic imaging consistent with acute pancreatitis pancreatic acidosis and reducing trypsin activity, although current
evidence suggests a modest morbidity/mortality benefit at most.21
Morphology Conversely, patients with acute pancreatitis due to hypercalcemia
Acute edematous Acute necrotizing pancreatitis should not undergo fluid resuscitation with calcium-containing LR
- Rare
interstitial pancreatitis given concerns of further exacerbating the underlying pancreatic
- Common - Necrosis of pancreas and injury and saponification of peripancreatic tissues.
- Diffuse inflammatory edema peripancreatic tissues
With regards to the rate, Gardner et. al demonstrated that those
Severity who received more than one third of their cumulative 72-hour IV
fluids within the first 24 hours experienced a reduction in per-
- No evidence of organ dysfunction sistent organ failure (35% vs 43%) and overall mortality (0% vs
Mild - Conservative management 18%) when compared to those who did not receive sufficient early
- Low morbidity and mortality fluid resuscitation.19 This reduction in morbidity afforded by early
- Local or systemic complications fluid resuscitation has been continually demonstrated in subse-
Moderate - Transient organ failure <48 hours quent studies.20 Many experts advocate for goal directed therapy,
- Varying morbidity and mortality targeted at addressing hypotension, tachycardia, elevated hemato-
crit (suggestive of hemoconcentration), elevated blood urea nitro-
- Persistent organ failure >48 hours gen (BUN), and ensuring adequate urine output. Trends in BUN
Severe
- High morbidity and mortality measured at admission, 24 hours, and 48
hours has been demonstrated to predict Acute Pancreatitis
Table 4: Table outlining acute pancreatitis definition, morphology and severity characteristics
mortality in acute pancreatitis, with those continued on page 10

Annals of B Pod 9
Acute Pancreatitis having a BUN of 20 mg/dL or higher on Local Complications
continued from page 9 admission having a mortality OR of 4.6; Peri-pancreatic Fluid Collections
furthermore, any increase in BUN 24 As discussed previously, there are two morphological classifi-
hours from admission confers an OR of 4.3 for mortality.22 As such, cations of acute pancreatitis, each of which is associated with a
many experts recommend fluid therapy be directed at decreasing unique pancreatic fluid collection. Acute edematous pancreatitis
the BUN within the first 24 hours of admission.13,23 Currently, may result in an acute peripancreatic fluid collection (APFC) and
guidelines from the American College of Gastroenterology recom- pseudocyst formation, while patients with acute necrotizing pan-
mend an infusion of 2.5 to 4 liters in the first 24 hours, with an creatitis may develop acute necrotic collection (ANC) and walled-
initial infusion rate of 250-500 mL/hr. While adequate fluid resus- off pancreatic necrosis (WOPN).
citation is a pillar of acute pancreatitis management, it is important
to remember that overly aggressive fluid resuscitation can increase An acute peripancreatic fluid collection typically develops early in
the risk for developing abdominal compartment syndrome. acute pancreatitis (within four weeks of symptom onset) and re-
fers to peripancreatic fluid without a well-defined wall and without
In summary, fluid resuscitation is paramount in acute pancreatitis, solid or necrotic contents. APFCs are at low risk of superimposed
early resuscitation is better than late resuscitation, therapy should infection, with the majority spontaneously involuting within 7-10
be targeted at decreasing BUN within the first 24 hours, and lactat- days.25 As such, APFCs do not typically require additional treat-
ed ringers may be a superior fluid choice. ment. When APFCs do persist beyond four weeks, however, they
frequently develop a defined wall and coalesce into a pancreatic
Antibiotics pseudocyst.
As our understanding of acute pancreatitis has evolved, the role
of prophylactic antibiotics has been hotly contested, in no small Similarly, for necrotizing pancreatitis, an acute necrotic collection
part secondary to the mixed and frequently contradictory evidence typically occurs within the first four weeks of insult and is defined
published in recent literature. A 2001 meta-analysis by Sharma and as a collection of fluid and necrotic tissue which lacks a well-de-
Howden evaluating prophylactic antibiotics in patients with acute fined wall. Despite superficial similarities to an APFC, an ANC is
necrotizing pancreatitis demonstrated a greater than 20% reduc- differentiated in that it develops following necrotizing pancreatitis
tion in the incidence of sepsis and a 12% reduction in mortality and contains necrotic tissue. Ultrasonography, both transcutane-
when compared to patients not receiving prophylactic antibiotics.16 ous and endoscopic, may be used to confirm the presence of solid
Curiously, despite the robust reduction in mortality, the same study material within the collection, distinguishing ANC from APFC.
showed no decrease in the incidence of developing a pancreatic Persistent necrotizing collections lasting greater than four weeks
infection. Subsequent meta-analyses published in 2008 and 2011 may organize into a cystic structure similar to a pancreatic pseudo-
failed to demonstrate a benefit of prophylactic antibiotic adminis- cyst, termed walled-off necrosis.
tration in reducing infection rates, incidence of multiorgan failure,
need for surgical intervention, or mortality.17,18 Compilations of Both pseudocysts and areas of walled-off necrosis present with
more recent literature seem to support this lack of demonstrable varying symptoms such as pain, fevers, chills, jaundice, or early
benefit.15 Current guidelines recommend against the routine use of satiety. In asymptomatic patients, pseudocysts are typically man-
prophylactic antibiotics for acute pancreatitis, regardless of mor- aged conservatively with routine imaging every 3-6 months un-
phology or severity, and suggest that they should not be utilized as til resolution or significant decrease in size. In one study by Cui,
part of management unless infection is objectively demonstrated. more than 80% of patients saw reduction or complete resolution of
their pseudocyst at one year.1 Supportive care for both pseudocysts
Pain and WOPNs also includes enteric feeding for nutritional support
Acute pancreatitis is associated with significant pain, and ade- with concomitant use of proton pump inhibitors and somatostatin
quate analgesia is an important consideration as patients may be analogues to decrease pancreatic secretions. When secreted, the
unwilling or unable to tolerate oral nutrition/hydration without pancreatic enzyme trypsinogen is activated into trypsin by enter-
satisfactory pain control. Opioid agents are frequently employed okinase in intestinal mucosa. Activated trypsin is then able to ac-
to this effect. Traditionally, providers were encouraged to avoid the tivate additional trypsinogen into more trypsin. Acute pancreatitis
use of morphine in acute pancreatitis due to the theoretical ‘risk’ results in widespread activation of pancreatic enzymes, triggering
of increased tone in the sphincter of Oddi, obstructing passage of a vicious cycle which leads to autodigestion and pancreatic dam-
biliary contents into the duodenal lumen. The use of meperidine age. Under this premise, inhibition of pancreatic secretions should
was encouraged as it was considered a non-contracting alterna- minimize the occurrence of autodigestion and forestall subse-
tive. This practice has been thoroughly refuted by recent literature, quent damage. Furthermore, somatostatin analogues may hasten
however, with one study actually demonstrating a greater effect on pseudocyst resolution by minimizing pancreatic secretions into
increasing common bile duct pressure with use of meperidine in the fluid collection.
comparison to morphine.24 Given its numerous side-effects and
black box warnings, the routine use of meperidine for analgesia In patients with clear symptoms, rapidly enlarging cysts, or dysreg-
has fallen from clinical practice. Instead, providers are encouraged ulated systemic responses to infected cysts, providers may consider
to optimize analgesia using appropriate doses of agents individu- drainage of pseudocystic structures to alleviate symptoms. Infect-
ally selected and titrated to the unique physiologic characteristics ed pancreatic necrosis or symptomatic sterile necrosis should also
of their patient. undergo drainage. There are several options for drainage including
endoscopic, percutaneous, or surgical. With recent advances in fi-
beroptic technology, endoscopic management has superseded both

10 Annals of B Pod
surgery and percutaneous techniques as the preferred option. A the exact etiology of thrombosis is unclear, it is theorized that clot
recent study has shown >90% success rate of endoscopic drainage formation may stem from local inflammation or mass effect from
with lower associated morbidity compared to other modalities; an- nearby peri-pancreatic fluid collections. A 2011 prospective study
other study that compared various approaches to drainage demon- by Gonzelez et al following 127 consecutive patients with acute
strated a 70% success rate with endoscopic techniques in contrast pancreatitis found that 20 patients had splanchnic venous throm-
to a 31% success rate with percutaneous treatment.3,4,5 Additionally, bosis and all were associated with severe, acute pancreatitis.12 In
percutaneous approaches were three times as likely to progress to affected patients, the splenic vein was most commonly implicated,
surgery as compared to endoscopic management.5 Unfortunately, followed by the portal vein and the superior mesenteric vein, re-
successful endoscopic management is predicated on several as- spectively.12 Of note, 19 of the 20 patients with splanchnic venous
sumptions: first, the fluid collection must be mature (completely thrombosis also had adjacent peri-pancreatic fluid collections. The
walled-off); in addition, the collection wall must be adherent to the sequelae of splenic vein thromboses include liver dysfunction, por-
bowel lumen to facilitate transluminal puncture into the pseudo- tal hypertension, and variceal formation. Supportive therapy of
cyst; and finally, the collection must be >6 cm to increase the like- the underlying pancreatitis is the mainstay of treatment; however,
lihood of successful to the cystic contents.2 The development of a extension of the clot into the portal vein or mesenteric veins with
pseudoaneurysm (discussed later) is an absolute contraindication resultant liver or bowel compromise may warrant anticoagulation.
for endoscopic drainage due to the risk of accidental vascular in-
jury and potential large-volume hemorrhage. For these reasons, Pseudoaneurysm
endoscopic drainage is not always a viable choice. It is also worth Approximately 10% of patients with pancreatic fluid collections
noting that, due to the nature of the contents may develop pseudoaneurysms. These can
of WOPN, they frequently require multiple Pancreatitis Treatment form independently as a primary pseudo-
or combined means for drainage, as endo- aneurysm due to direct vascular injury or by
scopic drainage alone has lower success rates Fluid Resuscitation arterial rupture into a pseudocyst, ultimately
in WOPN when compared to its pseudocyst Pain Management forming a pseudoaneurysm. Risk factors for
counterpart.4,6 pseudoaneurysm formation include peri-pan-
Pancreatitis Complications creatic fluid collections, sepsis, multi-organ
Infection failure, long term anticoagulation, underly-
Both ANC and WOPN are sterile on initial Local Complications ing vasculitis, necrotizing pancreatitis, and
formation but have the potential to become - Pseudocyst previous pancreatic necrosectomy.10 Pseudo-
infected. The rate of infection in ANC and - Necrosis aneurysms may expand rapidly and rupture
WOPN is notably higher than their edem- - Infection into the peritoneal cavity, retroperitoneum, or
atous non-necrotic counterparts, with ap- adjacent bowel with potentially catastrophic
proximately 1/3 of patients with pancreatic Vascular Complications consequences. Therefore, patients with rap-
necrosis developing infection.7 Despite this - Splanchnic venous thrombosis idly expanding pancreatic fluid collections, a
increased risk, prophylactic antibiotics are sudden drop in hemoglobin, or evidence of
- Pseudoaneursym
not routinely indicated given the potential gastrointestinal hemorrhage should raise sus-
adverse effects of broad-spectrum antibiosis Abdominal Compartment picion of possible pseudoaneurysm formation.
and difficulty in predicting infections due Syndrome Computed tomography with arterial phase
in part to the lack of correlation between contrast can be useful in detecting and eval-
extent of necrosis and risk of developing a Table 5: Table outlining acute pancreatitis management and uating pseudoaneurysms, though digital sub-
complications to consider
subsequent infection. When they occur, in- traction angiography remains the gold stan-
fections are most frequently monomicrobial secondary to an en- dard for diagnosis. Pseudoaneurysms most commonly develop in
teric organism, such as Escherichia, Pseudomonas, Klebsiella, or the splenic artery, though they may also occur within the hepatic
Enterococcus species. Signs of developing or fulminant pancreatic and gastroduodenal arteries.11 Intervention should occur rapidly
infections are consistent with those of traditional systemic infec- once identified, as the mortality from complications is exceedingly
tious response, typified by leukocytosis, fevers, and hemodynamic high. There are numerous techniques for management including
decompensation. The mainstay of treatment for infected pancreatic endovascular management (coiling or foam), ultrasound-guided
necrosis is IV antibiotics with or without debridement, with surgi- percutaneous thrombin injections, or open surgical management.
cal interventions tailored to the patient’s individual clinical course. Angiographic management is preferred as it is less invasive and al-
In patients who do not improve promptly with intravenous anti- lows easier access and more concise identification of the bleeding
biotics, necrosectomy (i.e., surgical debridement) is performed. vessels, which are frequently deep within the friable pancreatic pa-
In clinically stable patients, however, delaying debridement with a renchyma. However, angiography is reserved for relatively stable
prolonged course of antibiotics may reduce the extent of necrotic patients, and those who are unstable or who have failed angiogra-
tissue or potentially even completely resolve the infection, thereby phy often require surgical management.11
eliminating the need for surgical management entirely.
Abdominal Compartment Syndrome
Vascular Complications Abdominal compartment syndrome is defined as a sustained in-
Splanchnic Venous Thrombosis tra-abdominal pressure above 20 mmHg with new onset organ
Thrombosis of the splanchnic venous system, including the portal, failure. Patients with severe pancreatitis,
splenic, and superior mesenteric veins, has been identified in up those who underwent substantial fluid Acute Pancreatitis
to as many as 24% of patients with acute pancreatitis.8 Though volume replacement, with ascites, or continued on page 12

Annals of B Pod 11
Acute Pancreatitis venous potassium correction should not exceed 20 mmol/hour
continued from page 11 except for emergent situations where central venous access is avail-
able.9 Administration of potassium at rates exceeding 20 mmol/
those with significant peri-pancreatic edema are at higher risk of hour may cause cardiac toxicity, including arrhythmias and car-
developing abdominal compartment syndrome.13 For this reason, diac arrest. Patients should be monitored on a continuous cardiac
patients with severe pancreatitis or in the ICU should have regular monitor and the serum potassium level should be measured hourly
bladder pressure monitoring. Management is the same as that for when intravenous potassium is administered at rates exceeding 20
abdominal compartment syndrome due to other causes. mmol/hour. Additionally, infusion site checks should be conduct-
ed regularly as high concentrations administered via a peripheral
Summary line can cause phlebitis and pain.10 Identification and treatment of
Acute pancreatitis is a disease process frequently encountered in concurrent hypomagnesemia are also important because magne-
the emergency room and, when severe, can carry a high mortality. sium depletion impedes potassium repletion and can exacerbate
It is diagnosed by two of the following: lipase greater than three hypokalemia-induced rhythm disturbances.11,12 Dextrose contain-
times the upper limit of normal; signs and symptoms of acute pan- ing solutions can worsen hypokalemia and should not be used as
creatitis; or imaging findings. It can be characterized by morphol- the replacement fluid. All patients should have cardiac monitoring
ogy and severity. Gallstones are the most common cause of acute while potassium is being replaced intravenously.
pancreatitis in the United States, followed by alcohol and various
other etiologies. Management focuses on adequate fluid resuscita-
tion, pain control, and oral nutrition as tolerated. Notably, antibiot- Potassium Administration
ics are not standard of care in acute pancreatitis without proven in-
- Administer potassium at 10-20 mEq/h IV, 40mEq orally if able
fection. Complications of acute pancreatitis include peripancreatic
- Can administer potassium at 40 mEq/h with life-threatening
fluid collections, infection, abdominal compartment syndrome,
hypokalemia
and local vascular complications.
- Consider giving empiric 2g magnesium as patient will be unable
1.Cui, M. L., Kim, K. H., Kim, H. G., Han, J., Kim, H., Cho, K. B., ... & Kim, T. N. (2014). Incidence, risk factors and clinical course of to absorb potassium effectively if hypomagnesiumic
pancreatic fluid collections in acute pancreatitis. Digestive diseases and sciences, 59(5), 1055-1062.
2.Binmoeller, K. F. (2013). EUS-guided drainage of pancreatic fluid collections using fully covered self-expandable metal stents. Gas-
troenterology & hepatology, 9(7), 442.
3.Antillon, M. R., Shah, R. J., Stiegmann, G., & Chen, Y. K. (2006). Single-step EUS-guided transmural drainage of simple and com-
plicated pancreatic pseudocysts. Gastrointestinal endoscopy, 63(6), 797-803. Table 6: Recommendations on treating hypokalemia
4.Hookey, L. C., Debroux, S., Delhaye, M., Arvanitakis, M., Le Moine, O., & Devière, J. (2006). Endoscopic drainage of pancre-
atic-fluid collections in 116 patients: a comparison of etiologies, drainage techniques, and outcomes. Gastrointestinal endoscopy,

Summary
63(4), 635-643.
5.Keane, M. G., Sze, S. F., Cieplik, N., Murray, S., Johnson, G. J., Webster, G. J., ... & Pereira, S. P. (2016). Endoscopic versus percu-
taneous drainage of symptomatic pancreatic fluid collections: a 14-year experience from a tertiary hepatobiliary centre. Surgical
endoscopy, 30(9), 3730-3740. While hyperkalemia is the more commonly encountered and
6.Baron, T. H., Harewood, G. C., Morgan, D. E., & Yates, M. R. (2002). Outcome differences after endoscopic drainage of pancreatic
necrosis, acute pancreatic pseudocysts, and chronic pancreatic pseudocysts. Gastrointestinal endoscopy, 56(1), 7-17. feared complication of abnormal potassium homeostasis, hypoka-
7.Banks, P. A., & Freeman, M. L. (2006). Practice guidelines in acute pancreatitis. The American journal of gastroenterology, 101(10),
2379. lemia too can be devastating. When concerned for hypokalemia
8.Nadkarni, N. A., Khanna, S., & Vege, S. S. (2013). Splanchnic venous thrombosis and pancreatitis. Pancreas, 42(6), 924-931.
9.Balthazar, E. J. (2002). Acute pancreatitis: assessment of severity with clinical and CT evaluation. Radiology, 223(3), 603-613. always assess the cardiac and neurologic status, confirm the diag-
10.Sharma, P. K., Madan, K., & Garg, P. K. (2008). Hemorrhage in acute pancreatitis: should gastrointestinal bleeding be considered
an organ failure?. Pancreas, 36(2), 141-145. nosis with repeat labs if time/acuity permits, and initiate treatment
11.Barge, J. U., & Lopera, J. E. (2012). Vascular complications of pancreatitis: role of interventional therapy. Korean journal of radiol-
ogy, 13(Suppl 1), S45-S55. early once the diagnosis is made. Oral and intravenous potassi-
12.Gonzelez, H. J., Sahay, S. J., Samadi, B., Davidson, B. R., & Rahman, S. H. (2011). Splanchnic vein thrombosis in severe acute
pancreatitis: a 2‐year, single‐institution experience. HPB, 13(12), 860-864. um are the initial treatment. Simultaneous magnesium adminis-
13.Working, G. I., & APA, A. P. G. (2013). IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatol-
ogy: official journal of the International Association of Pancreatology (IAP)...[et al.], 13(4 Suppl 2), e1. tration should be considered particularly if magnesium levels are
14.Banks, P. A., Bollen, T. L., Dervenis, C., Gooszen, H. G., Johnson, C. D., Sarr, M. G., ... & Vege, S. S. (2013). Classification of acute
pancreatitis—2012: revision of the Atlanta classification and definitions by international consensus. Gut, 62(1), 102-111. unknown. All patients should have EKGs performed to assess for
15.Crockett, S. D., Wani, S., Gardner, T. B., Falck-Ytter, Y., Barkun, A. N., Crockett, S., ... & Gupta, S. (2018). American Gastroentero-
logical Association Institute guideline on initial management of acute pancreatitis. Gastroenterology, 154(4), 1096-1101. cardiac abnormalities. Initial efforts should be focused on replace-
16.Sharma, V. K., & Howden, C. W. (2001). Prophylactic antibiotic administration reduces sepsis and mortality in acute necrotizing
pancreatitis: a meta-analysis. Pancreas, 22(1), 28-31. ment and resuscitation but exploring the potential etiology of the
17.Wittau, M., Mayer, B., Scheele, J., Henne-Bruns, D., Dellinger, E. P., & Isenmann, R. (2011). Systematic review and meta-analysis of
antibiotic prophylaxis in severe acute pancreatitis. Scandinavian journal of gastroenterology, 46(3), 261-270. patients hypokalemia can serve to guide inpatient management.
18.Bai, Y., Gao, J., Zou, D. W., & Li, Z. S. (2008). Prophylactic antibiotics cannot reduce infected pancreatic necrosis and mortality
in acute necrotizing pancreatitis: evidence from a meta-analysis of randomized controlled trials. The American journal of gastroen-
terology, 103(1), 104.
19.Gardner, T. B., Vege, S. S., Chari, S. T., Petersen, B. T., Topazian, M. D., Clain, J. E., ... & Sarr, M. G. (2009). Faster rate of initial fluid
resuscitation in severe acute pancreatitis diminishes in-hospital mortality. Pancreatology, 9(6), 770-776. 1. Paice BJ, Paterson KR, Onyanga-Omara F, Donnelly T, Gray JM, Lawson DH. Record linkage study of hypokalaemia in hospitalized
20.Warndorf, M. G., Kurtzman, J. T., Bartel, M. J., Cox, M., Mackenzie, T., Robinson, S., ... & Gardner, T. B. (2011). Early fluid resusci- patients. Postgrad Med J. 1986;62(725):187-191.
tation reduces morbidity among patients with acute pancreatitis. Clinical gastroenterology and hepatology, 9(8), 705-709. 2. Lippi G, Favaloro EJ, Montagnana M, Guidi GC. Prevalence of hypokalaemia: the experience of a large academic hospital. Intern
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systemic inflammation compared with saline in patients with acute pancreatitis. Clinical Gastroenterology and Hepatology, 9(8), 3. Liamis G, Rodenburg EM, Hofman A, Zietse R, Stricker BH, Hoorn EJ. Electrolyte disorders in community subjects: prevalence and
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23.Janisch, N. H., & Gardner, T. B. (2016). Advances in management of acute pancreatitis. Gastroenterology Clinics, 45(1), 1-8. 6. Girish MP, Gupta MD, Mukhopadhyay S, Yusuf J, Sunil Roy TN, Trehan V. U wave: an important noninvasive electrocardiographic
24.Radnay, P. A., Brodman, E., Mankikar, D., & Duncalf, D. (1980). The effect of equi-analgesic doses of fentanyl, morphine, meperi- diagnostic marker. Indian Pacing Electrophysiol J. 2005 Jan 1;5(1):63-5.
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fluid collections. American Journal of Roentgenology, 190(3), 643-649. 8. Macdonald JE, Struthers AD. What is the optimal serum potassium level in cardiovascular patients? J Am Coll Cardiol.
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12. Millane TA, Ward DE, Camm AJ. Is hypomagnesemia arrhythmogenic? Clin Cardiol. 1992;15(2):103-108.
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Hypokalemia level, this can be used to estimate 14. Gennari FJ. Disorders of potassium homeostasis. Hypokalemia and
hyperkalemia. Crit Care Clin. 2002;18(2):273-288.
continued from page 3 the amount of potassium needed
to correct the patient’s hypokale-
mia. Oral potassium is the preferred route of administration with
To Learn more on Hypokalemia EKGs - turn to
intravenous potassium reserved for patients with ECG changes,
physical signs or symptoms of hypokalemia, inability to tolerate EKG Corner on the Back Cover
potassium by mouth or severe hypokalemia (<2.5 mEq/L). Intra-

12 Annals of B Pod
Traumatic Rupture
continued from page 7
tures and 17% for right-sided ruptures.11,12 Ultrasound can also liver, diaphragm, and lung.17 Diaphragmatic paralysis may de-
be used to evaluate the diaphragm, looking for discontinuity of velop as a result of phrenic nerve injury, which occurs most of-
the structure and herniation of the liv ten with high cervical spine or penetrating neck trauma, but can
also occur as a result of diaphragmatic tears. The contraction of
er or bowel loops; however, its use is not standardized and thus the diaphragm is responsible for 75-80 % of a healthy individ-
cannot be used to exclude the diagnosis.13,14 Furthermore, plain ual’s tidal volume, so if patient sustains an injury resulting in a
radiographs and ultrasound will largely depend on bowel con- paralyzed hemidiaphragm, then lung capacity may decrease as
tent herniation as an obvious sign of diaphragm rupture, but much as 20-30%. These patients may be eventual candidates for
several studies have postulated that positive pressure ventilation diaphragmatic plication.
in intubated patients will obscure this finding by inhibiting the The National Trauma Data Bank (NTDB) reports an overall
degree of herniation into the thoracic cavity. As such, providers mortality for patients with diaphragmatic injury of 25%.2 In a
must be cautious when using these imaging modalities to rule study using data from NTDB, patients with blunt diaphragmat-
out diaphragmatic injury in intubated and mechanically venti- ic injury had both a significantly higher mortality rate (19.8%
lated patients. v 8.8%) and higher rate of pulmonary complications (14.8% v.
6.6%) compared to those with penetrating trauma.3 If patient
In general, CT imaging is more useful in detecting these inju- presentation is delayed such that abdominal contents become
ries, though studies attribute a variable sensitivity and specific- incarcerated, then mortality increases to 20%, and mortality
ity to the modality of 61-87% and 72-100%, respectively. There further increases to 40-57% if bowel strangulation develops.18
are several radiographic findings that can assist with making
the diagnosis. The discontinuity sign, or obvious discontinua- Summary
tion of the normal curvature of the diaphragm on imaging, and Traumatic diaphragmatic rupture is a relatively rare injury that
diaphragmatic thickening sign are the most common radiologic may be present in both blunt and penetrating trauma patients
findings. The collar sign (hour-glass constriction at the level of and frequently occurs in conjunction with other thoracic and
the injured diaphragm as herniated hollow viscus is forced into abdominal injuries. It is a challenging diagnosis to make, ne-
the thoracic cavity) and dependent viscera signs (found in su- cessitating a high index of suspicion based on injury mecha-
pine patients where herniated hollow viscous are found depen- nism, exam, and associated injuries. Chest radiography has
dent along the posterior ribs) were almost exclusively found in poor sensitivity in detecting injuries, so CT is the primary im-
blunt trauma patients, and the dangling diaphragm sign (free aging modality used to diagnose diaphragmatic injury. With-
edge of the torn diaphragm curves in on itself) and organ her- out intervention, the size of the diaphragmatic defects generally
niation signs were seen more commonly in patients with blunt increases over time. Herniation of abdominal viscera with sub-
trauma. Unfortunately, CT imaging still has a wide range of sequent ischemia and infarction is the most common complica-
sensitivity, especially if the injury is on the right where homo- tion of traumatic diaphragmatic ruptures; however, the injury
geneity between the liver and diaphragm can obscure potential can also precipitate important pulmonary complications, dia-
findings.15 The gold standards for diagnosing diaphragmatic phragmatic paralysis, and fistulas.
injuries remain more invasive techniques such as diagnostic
laparoscopy, thorascopy, or open surgical exploration.16
1. Trauma, 6, Feliciano, DV, Mattox, KL, Moore, EF (Eds), McGraw-Hill, 2008.
2. National Trauma Data Base. American College of Surgeons 2000-2004. https://ntdbdatacenter.com/ (Accessed on January
Management 01, 2005).
3. Fair KA, Gordon NT, Barbosa RR, Rowell SE, Watters JM, Schreiber MA. Traumatic diaphragmatic injury in the American
Management of patients with diaphragm injury depends large- College of Surgeons National Trauma Data Bank: a new examination of a rare diagnosis. Am J Surg. 2015;209(5):864.
4. Lochum S, Ludig T, Walter F Imaging of diaphragmatic injury: a diagnostic challenge? Radiographics. 2002; 22:103-108
ly on timing of diagnosis, laterality and extent of injury. Ac- 5. Waldhausen JA, Kilman JW, Helman CH, et al. The diagnosis and management of traumatic diaphragmatic injuries of the
diaphragm including the use of marlex prostheses. J Trauma 1966;6:332-43.
cording to the Eastern Association for the Surgery of Trauma 6. de la Rocha AG, Creel RJ, Mulligan GW, et al. Diaphragmatic rupture due to blunt abdominal trauma. Surg Gynecol Obstet
1982;154:175-80.
(EAST) guidelines, right-sided injuries may require repair, but 7. Asensio JA, Petrone P Diaphragmatic injury. Current Surgical Therapy. 2004; :946-955
8. Moore EE, Malangoni MA, Cogbill TH, Shackford SR, Champion HR, Jurkovich G, McAninch JW, Trafton PG. Organ injury
if small and asymptomatic with a hemodynamically stable pa- scaling IV: Thoracic vascular, lung, cardiac, and diaphragm. J Trauma – Injury, Infection, and Critical Care. 1994; 36 (3):
299-300
tient, supportive care and nonoperative observation may be a 9. Williams M, Carlin AM, Tyburski JG, Blocksom JM, Harvey EH, Steffes CP, Wilson RF. Predictors of mortality in patients
with traumatic diaphragmatic rupture and associated thoracic and/or abdominal injuries. Am Surg. 2004;70(2):157.
feasible treatment option. Conversely, the majority of left-sided 10. Shanmuganathan K, Killeen K, Mirvis SE, White CS. Imaging of diaphragmatic injuries. J Thorac Imaging. 2000;15(2):104.
11. Gelman R, Mirvis SE, Gens D. Diaphragmatic rupture due to blunt trauma: sensitivity of plain chest radiographs. AJR Am
diaphragmatic injuries will require repair, though it may be de- J Roentgenol. 1991; 156; 51-57.
12. Killeen KL, Mirvis SE, Shanmuganathan K. Helical CT of diaphragmatic rupture caused by blunt trauma. AJR Am J Roent-
layed depending on extent and severity of associated injuries.16 genol. 1999;173 (6): 1611-6.
13. Blaivas M, Brannam L, Hawkins M, Lyon M, Sriram K. Bedside emergency ultrasonographic diagnosis of diaphragmatic
Regardless of degree of injury, if diaphragm injury is diagnosed rupture in blunt abdominal trauma. Am J Emerg Med. 2004;22(7):601.
14. Gangahar R, Doshi D. FAST scan in the diagnosis of acute diaphragmatic rupture. Am J Emerg Med. 2010;28(3):387.e1.
in the ED, the first steps include decompressing the stomach 15. Panda A, Kumar A, Gamanagatti S, Patil A, Kumar S, Gupta A. Traumatic diaphragmatic injury: a review of CT signs and
the difference between blunt and penetrating injury. Diagn Interv Radiol. 2014;20(2):121.
with a gastric tube and providing supportive care. 16. McDonald AA, Robinson BRH, Alarcon L, Bosarge PL, Dorion H, Haut ER, Juern J, Madbak F, Reddy S, Weiss P, Como JJ.
Evaluation and management of traumatic diaphragmatic injuries: A Practice Management Guideline from the Eastern Associa-
tion for the Surgery of Trauma. J Trauma Acute Care Surg. 2018;85(1):198.
17. Petrone P, Leppaniemi A, Inaba K, Soreid e K, Asensio JA. Diaphragmatic injuries: challenges in the diagnosis and man-
Mortality rates from diaphragmatic injury depend on the mech- agement. Trauma. 2007;9:227–36
18. Sullivan RE. Strangulation and obsturciton in diaphragmatic hernia due to direct trauma. Report of two cases and review of
anisms and presence of associated injuries. In addition to the the English literature. J Thorac Cardiovasc Surg. 1966; 52 (5): 725.

aforementioned complications of bowel herniation and possible


strangulation of abdominal organs, other possible complications
include diaphragmatic paralysis, pulmonary complications, and
biliary fistulas which can evolve with combined injury to the
Annals of B Pod 13
Malaria days to months after the initial suspicion is high after an initial negative smear, it is recommended
continued from page 5 exposure. As demonstrated in this that peripheral blood smears be repeated every 12 hours until there
case, signs and symptoms of vivax are three negative smears, as the first smear is negative in up to 10%
and ovale infection can present even years later due to activation of of patients.8,9,14 Frequent finger stick blood glucose may be helpful
residual hypnozoites. as well given the frequency of hypoglycemia in malaria. Regardless,
in highly suspicious cases, absence of parasitemia should not delay
Fever and headache are two of the most common symptoms in pa- initiation of antimalarial therapy.9 The CDC Yellow Book is also a
tients with malaria. Otherwise, initial symptoms of uncomplicated useful resource for both patients and clinicians, as it contains the
malaria are non-specific and may include malaise, lightheadedness, most up-to-date travel health guidelines, including disease-specific
chills, myalgias, arthralgias, cough, abdominal pain, anorexia, and guidance regarding vaccination, chemoprophylaxis, and preventive
nausea. On examination, providers may find evidence of anemia, measures.15
splenomegaly, hepatomegaly, jaundice, in addition to vital sign ab-
normalities such as fever, tachycardia, and tachypnea. Given the Management and Treatment
breadth and variability of presentation, it is unsurprising that un- Once the diagnosis of malaria is confirmed, even without identifying
complicated malaria is often misdiagnosed as influenza, hepatitis, a specific species, initiation of prompt, appropriate antimalarial ther-
gastroenteritis, or meningitis.9,10 apy and supportive care are of paramount importance. Treatment is
determined by the severity of presentation, species of malaria, and
All patients who are suspected of having malaria should be assessed region-specific incidence of antimalarial resistance stemming from
for features of severe malaria, which differs between adults and chil- where the patient was likely exposed. If the species is not yet known,
dren and necessitates a different treatment regimen. P. falciparum it is reasonable to treat the patient for suspected P. falciparum infec-
and P. knowlesi are the most likely to progress to severe malaria. Se- tion and deescalate as appropriate.
vere malaria is thought to develop in part from the sequestration and
cytoadherence of infected red blood cells in smaller caliber vascu- For uncomplicated falciparum malaria, almost all patients should be
lature. Essentially, red blood cells become adherent to the walls of initiated on monotherapy with either atovaquone-proguanil (Malar-
capillaries, precipitating peripheral and cerebral hypoxia, capillary one) or artemether-lumefantrine (Coartem), as both agents remain
leakage, cytokine-driven inflammatory response, and multisystem effective in spite of the increasing prevalence of chloroquine-resistant
organ dysfunction. P. falciparum. Alternative, and less commonly used, agents include
artesunate-mefloquine, artesunate-amodiaquine, and dihydroar-
Clinical findings of severe malaria include altered consciousness temisinin-piperaquine. Given the potential teratogenicity of the
with or without seizures, acute respiratory distress syndrome, hy- aforementioned agents during organogenesis, uncomplicated P. fal-
potension, metabolic acidosis, acute kidney injury, hemoglobinuria ciparum malaria occurring during the first trimester is treated with
(“blackwater fever” from high parasitemia), hepatic failure with or quinine and clindamycin. In the second and third trimesters, howev-
without jaundice, coagulopathy or disseminated intravascular coagu- er, women can be treated with the same medication regimens used
lation, severe anemia (hemoglobin < 7 g/dL) or massive intravascular for non-pregnant patients. P. knowlesi should be treated in the same
hemolysis, and hypoglycemia. The presence of any one of these fea-
tures constitutes severe malaria.8,11,12 In children with severe malaria,
respiratory distress, anemia, convulsions and hypoglycemia are more Antibiotics for Malarial Infections
common. Conversely, pulmonary edema, acute respiratory distress
syndrome, and renal failure rarely occur in children, but are present P. falciparum
in over half of all adult cases of severe malaria. In patients with severe P. knowlesi
malaria, case fatality rates range between 5-30%.9
Most common: Less common:
Patients with cerebral malaria will present with impaired conscious- Atovaquone-proguanil (Malarone) Artesunate-mefloquine
ness, delirium, and/or seizures. Focal neurologic signs and symptoms Artemether-lumefantrine (Coartem) Artesunate-amodiaquine
are unusual.8,13 Cerebral malaria is a medical emergency because of Dihydroartemisinin-piperaquine
its propensity to rapidly progress to coma and death. Even with treat- Pregnancy:
ment, mortality in patients with cerebral malaria is estimated at 15- First trimester: quinine and clindmaycin
20%.8 Second trimester: treat with non-pregnant regimen

Evaluation and Diagnosis


In light of malaria’s non-specific clinical presentation, patients should P. malariae P. vivax
undergo a broad work-up, including blood cultures, CBC, BMP, vP. ovale
LFTs, PT/INR, VBG, thick and thin peripheral blood smears, as well
as non-contrast computed tomography of the head and a lumbar Chloroquine Chloroquine + Primaquine* or Tafenoquine*
puncture to evaluate for meningitis or overt intracranial patholo-
*prevent relapsing malaria due to dormant hypnozoite
gy. Malaria should be confirmed by either microscopy, which is the
activation
gold standard, or by rapid diagnostic testing. A thick blood smear
*can precipitate hemolytic anemia in G6PD deficiency
assesses presence of the parasite whereas the thin smear facilitates
identification of the species and percent parasitemia. A parasite load
Table 7: Treatment regimens for malaria depending on speciation and population
>4% parasitized red blood cells indicates severe malaria. If index of

14 Annals of B Pod
manner as falciparum given its propensity to cause severe infection. cence in seeking care. Thwing et al. estimated that fewer than half
Patients with uncomplicated, confirmed P. vivax, P. malariae, or P. of those who suffer severe malaria are able to reach a health facility
ovale infection can be treated with chloroquine unless the patient and, assuming a case-fatality rate of 90% at home and 20% in hospi-
has suspected exposure to chloroquine-resistant P. vivax. Patients tal, estimate the global annual incidence of severe malaria to be ap-
with P. vivax or P. ovale should also receive primaquine or the newly proximately 2 million.19 As such, it is important to carefully screen
FDA-approved tafenoquine to prevent relapsing malaria that occurs patients for signs and symptoms consistent with severe malaria in
due to dormant hypnozoite activation. Of note, both primaquine and these settings and to escalate treatment to parenteral antimalarials as
tafenoquine can precipitate hemolytic anemia in patients with G6PD appropriate and if available.
deficiency, so admission and testing are recommended prior to initi-
ation of this drug. Finally, the prevalence of antimalarial resistance varies significantly
geographically. P. falciparum is almost entirely resistant to chloro-
Patients with severe malaria, including women in all trimesters of quine and antifols, so the aforementioned artemisinin-based com-
pregnancy, require parenteral artesunate. Though artesunate, qui- bination treatments are recommended as first-line treatment for
nine, and quinidine may all be administered parenterally, artesunate uncomplicated malaria. An unfortunate and evolving challenge in
has proven superior in reducing mortality in endemic populations. malaria treatment is the increasing prevalence of substandard and
Furthermore, quinine therapy can exacerbate the hypoglycemia that falsified antimalarials. A 2017 World Health Organization report es-
often accompanies severe malaria, especially in pregnancy women. timated that at least 69,000 individuals die as a result of reduced ef-
Quinidine is associated with substantial cardiotoxicity, ventricular fectiveness, substandard or falsified antimalarials each year.20 Global
arrhythmias, QT prolongation, and hypotension. Patients with hy- surveillance programs are working to address the issue, starting with
potension or acidosis should receive cautious fluid resuscitation at greater scrutiny of the medication supply chain.
the risk of volume overload and pulmonary edema. Benzodiazepines
are an appropriate first line treatment for seizures. Given the associ- Ultimately, malaria remains one of the foremost global health prob-
ation of severe malaria with concomitant bacterial sepsis, most often lems, causing tremendous morbidity, mortality, and socioeconomic
with nontyphoidal Salmonella, patients with cerebral malaria should distress in endemic regions. However, the global community contin-
receive concomitant broad-spectrum antibiotics pending negative ues to levy incredible resources and attention not only to the treat-
blood culture results and clinical improvement.16 Information on ment of malaria, but also to innovative means of preventing its trans-
appropriate dosing and susceptibility of infecting parasites is avail- mission – from malaria hot spot targeting to impregnated bed nets
able through the CDC and should be referenced as treatment is ini- that target the parasite rather than the vector.
tiated.
Summary
The need to admit all patients with P. falciparum or unidentified Plas- Malaria is a devastating disease that exacts a tremendous toll on hu-
modium species has been a point of controversy. There have been man health and productivity worldwide. Cases in the U.S. are ob-
attempts to define triage criteria for patients requiring admission ver- served among those who have lived or traveled in endemic regions,
sus those appropriate for outpatient therapy; however, given Amer- but diagnosis requires a high index of suspicion as the symptoms can
ican providers’ relative inexperience with malaria and the potential be non-specific. A thorough travel history – including places visit-
for patients with P. falciparum to rapidly deteriorate, the CDC advis- ed, malaria prophylaxis taken, and previous infection – is important.
es admission for these patients. This allows providers to tailor spe- Peripheral blood smears detailing presence of malaria, percent par-
cies-specific therapy, ensure that the medication is tolerated by the asitemia, and speciation, are key to both diagnosis and appropriate
patient, and observe for clinical improvement or deterioration.17 Re- treatment. In patients diagnosed with P. falciparum or P. knowlesi
gardless of severity, all cases of malaria and treatment thereof should malaria or suspected of having severe malaria, prompt initiation of
be discussed in consultation with Infectious Disease clinicians to en- antimalarial therapy is critical as these patients can decompensate
sure appropriate dosing, follow-up, and surveillance reporting. rapidly.

Global Perspective 1 Malaria’s Impact Worldwide. https://www.cdc.gov/malaria/malaria_worldwide/impact.html. Accessed on 3/12/2019.


For health care providers who work with patients in endemic re- 2 Malaria. https://www.who.int/news-room/fact-sheets/detail/malaria. Accessed on 3/12/2019.
3 Mace, KE, Arguin PM, Tan KF. Malaria Surveillance – United States, 2015. MMWR Surveillance Summary. 2018; 67 (7): 1-28.
gions, it is useful to be aware of the variances in presentation, eval- 4 Snow RW, Guerra CA, Noor AM, Myint HY, Hay SI. The global distribution of clinical episodes of Plasmodium falciparum malaria.
Nature. 2005; 434 (7030): 214.
uation, and treatment of malaria. Rapid diagnostic tests (RDTs) are 5 Price RN, Tjitra E, Guerra CA, Yeung S, White NJ. Anstey NM. Vivax malaria: neglected and not benign. American Journal of Tropical
Medicine and Hygiene. 2007; 77 (6 Supplementary): 79.
increasingly available in endemic countries and may be employed in 6 Mueller I, Zimmerman PA, Reeder JC. Plasmodium malariae and Plasmodium ovale – the “bashful” malaria parasites. Trends in Par-
asitology. 2007; 23 (6): 278.
patients with suspected malarial exposures. These tests can detect the 7 White NJ. Plasmodium knowlesi: the fifth human malaria parasite. Clinical Infectious Disease. 2008; 46 (2): 172.
8 Malaria: Biology. https://www.cdc.gov/malaria/about/biology/index.html. Access on 3/13/2019.
presence of malaria parasite using a finger-prick blood sample and, 9 Walker NF, Nadjm B, Whitty CJ. Special Situations: Malaria. Medicine. 2014; 42 (2): 100-106.
10 Molyneaux, Malcolm. Malaria. In Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. Eds. Judith E. Tintinalli et al.
depending on design, may variably detect one or multiple species. New York, NY: McGraw-Hill, 2016, http://accessmedicine.mhmedical.com/content.aspx?bookid=1658&sectionid=109413077.
11 Treatment of Malaria: Guidelines for Clinicians (United States). https://www.cdc.gov/malaria/diagnosis_treatment/clinicians2.html.
Malaria RDTs provide a useful and relatively reliable alternative to Accessed on 3/15/2019.
12 Mung’Ala-Odera V, Snow RW, Newton CR. The burden of neurocognitive impairment associated with Plasmodium falciparum malaria
diagnosis if microscopy is not readily available, though they do not in sub-saharan Africa. American Journal of Tropical Medicine and Hygiene. 2004; 71 (2 Supplementary); 63.
13 Severe Malaria. Tropical Medicine & International Health. 2014; 19 Supplementary: 7-131.
always provide information about species or degree of parasitemia. 14 Helman, A, Meshkat, N, Muller, M. Fever in the Returning Traveler. Emergency Medicine Cases. March, 2016. https://emergencymed-
icinecases.com/fever-returning-traveler/. Accessed on 3/14/2019.
15 Centers for Disease Control and Prevention. CDC Yellow Book 2018: Health Information for International Travel. New York: Oxford
University Press; 2017.
Patients may present at a later, more severe stage of their disease 16 Ashley EA, Aung PP, Woodrow CJ. Malaria. The Lancet. 2018; 391: 1608-1621.
17 Griffith KS, Lewis LS, Mali S. Treatment of Malaria in the United States: A Systematic Review. JAMA. 2007; 297 (20): 2264-2277.
course, which can present another challenge for providers operating 18 How malaria RDTs work. World Health Organization. https://www.who.int/malaria/areas/diagnosis/rapid-diagnostic-tests/about-rdt/
en/. Accessed on 3/29/2019.
in endemic regions. Patients may experience significant barriers to 19 Thwing J, Eisele TP, Steketee RW. Protective efficacy of malaria case management and intermittent preventive treatment for preventing
malaria mortality in children: a systematic review for the Lives Saved Tool. BMC Public Health. 2011; 11(Suppl 3), S14.
accessing care secondary to local conflict, displacement, logistical 20 A study on the public health and socioeconomic impact of substandard and falsified medical products. Geneva: World Health Or-
ganization; 2017.
and economic barriers, poor infrastructure, and sociocultural reti-

Annals of B Pod 15
E G
focus
Matthew Scanlon, MD Figure 2: EKG depicting biphasic T wave and U wave that can be found as early changes in hypo-
University of Cincinnati R4 kalemia.

An elderly male presents to the emergency department with com-


plaints of dehydration after several days of profuse, watery diar- hypokalemia, emergency providers should act promptly to replete
rhea and emesis. The patient complains of persistent nausea even the patient's potassium stores. Magnesium supplementation is
after treated with a 5-HT3 antagonist and is written for 1.25 mg of often administered concomitantly with potassium given the high
intravenous droperidol. Minutes after receiving the medications, concurrence of hypomagnesemia with hypokalemia. Further-
the patient becomes diaphoretic and complains of severe chest more, patients' hypokalemia may reprove refractory to repletion
pain before becoming unresponsive. Cardiac monitoring reveals without magnesium, possibly secondary to magnesium-mediated
polymorphic, wide-complex tachycardia. The patient is defibril- resorption of potassium from the distal renal tubule. QT-pro-
lated once with return of spontaneous circulation. A subsequent longing agents and medications that reduce extracellular potas-
12-lead EKG reveals pronounced U-waves and a QTc of 640 ms. sium stores should be used judiciously and with caution. Tachy-
The patient's bloodwork returns with a serum potassium of 2.4 dysrhythmias should be ablated with electrical cardioversion/
mEq/L. defibrillation; patients with persistent or recurrent episodes of
polymorphic ventricular tachycardia may benefit from overdrive
Hypokalemia is a metabolic derangement marked by abnormally pacing, given the rate-dependent shortening of the QT-interval.
low serum concentrations of the potassium ion, typically defined Antiarrhythmic medications should be used with extreme caution
as <3.5 mEq/L. Numerous pathologic processes may precipitate as many also prolong the QT-interval and decrease heart rate,
hypokalemia, but common causes include gastrointestinal volume paradoxically increasing the risk of early afterdepolarization (the
loses (e.g., emesis, diarrhea, short gut syndrome), prolonged or so-called "R on T phenomenon").
high-dose diuretic use, malnutrition, and iatrogenic causes (such
as the use of beta-adrenoreceptor agonists and insulin). Found
primarily within the cytosol of both cardiomyocytes and somatic
cells, potassium plays an important role in re-establishing the
transmembrane potential necessary for normal conduction of
electromechanical impulses through the heart (as well as neurons
and myocytes). Consequently, severe reductions in potassium
stores may lead to problems with cellular repolarization.

Electrocardiographically, hypokalemia first manifests as flattening


or inversion of T-waves. With more severe loses (typically <3.0
mEq/L), patients may evince QT-prolongation, the evolution of Figure 3: EKG depicting ventricular dysrhythmias that can be found in severe hypokalemia. EKG
courtesy of Creative Commons SA-4.0 via LIfeinTheFastLane
U-waves (most notably in the precordial leads), and even ventric-
ular extrasystoles. Hypokalemia below 2.3 mEq/L is associated
1.Widimsky, P. (2008). Hypokalemia and the heart. e-Journal of Cardiology Practice, 7(9).
with increased risk of polymorphic ventricular tachydysrhythmias 2.Kjeldsen K. (2010). Hypokalemia and sudden cardiac death. Experimental and clinical cardiology, 15(4), e96–e99.
3.Chua, C. E., Choi, E., & Khoo, E. Y. H. (2018). ECG changes of severe hypokalemia. QJM: An International Journal of Medicine,
(e.g., torsades de pointes, ventricular fibrillation) 111(8), 581–582.
4.Levis, J. (2012). ECG Diagnosis: Hypokalemia. The Permanente Journal, 16(2).
5.Huang, C.-L., & Kuo, E. (2007). Mechanism of Hypokalemia in Magnesium Deficiency. Journal of the American Society of
Nephrology, 18(10), 2649–2652.
On identifying patients with electrocardiographic stigmata of

Annals of B Pod is always looking


Submitted B Pod Cases
Case Providers
for interesting cases to publish! Pancreatic Pseudocyst Baez/Bryant
White Dot Syndrome Banning/Goel
Please submit cases via EPIC In Spindle Cell Carcinoma Ventura/Thompson
Basket message to Dr. David Ovarian Torsion Laurence/Benoit
Habib. Make sure to include the Conversion Disorder Liebman/Knight
R1/R4 involved in the case. Meningitis Habib/Campbell

16 Annals of B Pod

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