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CASE REPORT Open Access
Ascariasis and hyperosmolar hyperglycemic
state: a surprising ultrasound finding in the
emergency department
Giles N. Cattermole* and Jean-Paul Nzabandora
Abstract
Background: We report the ultrasound finding of ascariasis in a patient with hyperosmolar hyperglycemic state
(HHS). Although ascariasis is common in low-resource settings, there has been no previous report associating
ascariasis with HHS.
Case presentation: A 26-year-old Rwandan man was admitted to the emergency department in coma, with a
glycemia of 600 mg/dl. He was resuscitated with fluids, intubated and ventilated, and treated with insulin and
antibiotics. On day 3, an ascaris worm was passed via his nasogastric tube, and abdominal ultrasound revealed a
heavy worm load. He was treated with albendazole and eventually made a full recovery.
Conclusions: This is the first report of ascariasis as a potential cause of HHS, and we recommend that emergency
practitioners consider early abdominal ultrasound in patients with hyperglycemic emergencies in areas with a high
prevalence of ascariasis.
Keywords: Ascariasis, Ultrasonography, Diabetes complications
Background
Ascaris lumbricoides is an intestinal parasite common in
many low-income countries, associated with poor sanita-
tion [1]. Although over a billion people worldwide are
affected, it is still considered a neglected tropical disease
[2]. Adults with ascariasis are often asymptomatic, but
massive worm loads can cause intestinal or biliary ob-
struction, especially in children. Complications of ascaris
infestation also include pancreatitis, hepatic abscess, and
encephalitis.
Rwanda has a high prevalence of ascariasis. The most
recent nationwide study of over 8000 children found a
prevalence of 38.6%. In some rural districts, this rises to
over 50%. Despite treatment programs, transmission and
re-infection continues throughout Rwanda [3].
We report the ultrasound findings of ascariasis in a patient
with hyperosmolar hyperglycemic state (HHS). There has
been no previous report associating ascariasis with HHS.
Case presentation
A comatose 26-year-old Rwandan man was admitted to the
emergency department (ED) at the University Teaching
Hospital in Kigali, the capital city of Rwanda. He was hyp-
oxic, tachypneic, and tachycardic, but normotensive, with a
GCS of 6/15. Glycemia was 600 mg/dl (33.3 mmol/l). Initial
treatment included fluid resuscitation, intubation, and ven-
tilation. Temperature measurement and point-of-care
blood gas analysis were not available in the department at
that time. Urinary ketones were negative. A presumed diag-
nosis of HHS was made, and insulin infusion was started as
well as broad-spectrum antibiotics. No beds were available
in the intensive care unit, so he was managed for several
days in the ED. There was no significant past medical or
drug history.
Initial laboratory results included a mildly raised white
cell count, with normal electrolytes. He was HIV-
negative. There was no bacterial growth in blood cul-
tures, CSF, or urine. Chest X-ray and CT brain with con-
trast were both normal.
On day 3, a 30-cm adult female ascaris worm was as-
pirated from his nasogastric tube (Fig. 1), and abdominal
ultrasound revealed a heavy worm load (Fig. 2,
* Correspondence: giles@cattermole.org.uk
Emergency Department, Centre Hospitalier Universitaire de Kigali, University
of Rwanda, Butare, Rwanda
International Journal of
Emergency Medicine
© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made.
Cattermole and Nzabandora International Journal of Emergency Medicine  (2017) 10:12 
DOI 10.1186/s12245-017-0138-7
Additional file 1: Video 1 and Additional file 2: Video 2):
several intra-luminal echogenic tubular structures exhi-
biting slow curling movements were seen in the small
bowel. He was treated with albendazole and made a full
recovery. No other precipitant for his HHS was identi-
fied, and he was discharged with a new diagnosis of type
2 diabetes mellitus, on metformin and glibenclamide.
Conclusions
HHS is most commonly precipitated by infection [4]. In
this case, no infection was identified other than the
heavy infestation with ascaris. We conclude therefore
that this might have been the significant contributory
factor in the patient’s development of HHS. It is however
possible that the HHS was precipitated by another infec-
tion, which itself might have been secondary to ascaria-
sis infestation. In our hospital, patients do not receive
investigations until paid for in advance. Our patient had
no access to money and depended on social services
agreeing to fund each investigation. This meant that all
our tests were significantly delayed, and it is possible
that our failure to identify alternative infection was due
to empiric treatment with broad-spectrum antibiotics. It
is also possible that the HHS occurred de novo, inde-
pendent of the ascariasis. However, whether ascariasis
was the ultimate or penultimate cause of the HHS, or
merely associated with it, it needed to be identified and
treated.
Ultrasound has been recommended elsewhere as a
helpful initial diagnostic tool to diagnose suspected as-
cariasis, especially where stool analysis for eggs is not
available. Characteristic sonographic findings are de-
scribed as a “winding highway” or “railway track” of par-
allel lines on longitudinal scans, or a “target” or “bull’s
eye” appearance on transverse scans. Live worms show
characteristic slow, pendular, non-directional move-
ments [5], as we have demonstrated. In our case, we ob-
tained clear images using the standard abdominal probe
(3.5 MHz). However, better images might be obtained
with a linear 5–10 MHz probe if the patient’s morph-
ology permits [6]. Ultrasound can also demonstrate
some of the complications of ascariasis, including free
fluid from perforation, bowel obstruction, and hepatic
abscess.
Because of the financial difficulties many patients have
in paying for formal imaging, our department routinely
uses bedside ultrasound for a wide spectrum of presen-
tations. This case demonstrated its potential for identify-
ing an important infection in a critically ill patient.
Our patient lived in Kigali, the capital of Rwanda,
which has a lower prevalence of ascariasis (<20%), but
his family home was in a high prevalence district (>50%)
[3]. In settings like ours, emergency practitioners should
have a high index of suspicion that the patient might be
infected. Ascariasis infection should be treated even in
isolation, but it is especially important to recognise and
treat if it is a potential cause or an exacerbation of a life-
threatening complication. We therefore advise that
emergency practitioners consider early abdominal ultra-
sound in patients with hyperglycemic emergencies in
areas with a high prevalence of ascariasis.
Additional files
Additional file 1: Video S1. Abdominal ultrasound scan. (MP4 2529 kb)
Additional file 2: Video S2. Abdominal ultrasound scan. (MP4 2945 kb)
Abbreviations
CSF: Cerebrospinal fluid; ED: Emergency department; GCS: Glasgow Coma
Score; HHS: Hyperosmolar hyperglycemic state
Funding
There was no funding for this case report.
Authors’ contributions
Both authors were involved in the management of the case. JPN reviewed
the notes and images. GC did the literature review and wrote the final
manuscript. Both authors read and approved the final manuscript.
Fig. 1 Ascaris worm
Fig. 2 Abdominal ultrasound scan
Cattermole and Nzabandora International Journal of Emergency Medicine  (2017) 10:12 Page 2 of 3
Competing interests
The authors declare that they have no competing interests.
Ethics approval and consent to participate
Signed consent was obtained from the patient’s “garde-malade” (responsible
relative), as is customary and good practice in this setting.
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in
published maps and institutional affiliations.
Received: 2 December 2016 Accepted: 15 March 2017
References
1. Crompton DWT. Ascaris and ascariasis. Adv Parasitol. 2001;48:285–374.
2. Dold C, Holland CV. Ascaris and ascariasis. Microbes Infect. 2011;13:632–7.
3. Rujeni N, Morona D, Ruberanziza E, Mazigo HD. Schistosomiasis and soil-
transmitted helminthiasis in Rwanda: an update on their epidemiology and
control. Infect Dis Poverty. 2017;6:8.
4. Pasquel FJ, Umpierrez GE. Hyperosmolar hyperglycemic state: a historic
review of the clinical presentation, diagnosis, and treatment. Diabetes Care.
2014;37:3124–31.
5. Umetsu S, Sogo T, Iwasawa K, Kondo T, Tsunoda T, Oikawa-Kawamoto M,
KomatsuH IA, Fujisawa T. Intestinal ascariasis at pediatric emergency room
in a developed country. World J Gastroenterol. 2014;20:14058–62.
6. Thapa NB. Ultrasound diagnosis of intestinal ascariasis. Glob J Med Res-D.
2014;14. http://medicalresearchjournal.org/index.php/GJMR/article/view/596/
513.
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Ascariasis and hyperosmolar hyperglycemic state: a surprising ultrasound finding in the emergency department

CASE REPORT Open Access
Pembrolizumab for metastatic melanoma
in a renal allograft recipient with
subsequent graft rejection and treatment
response failure: a case report
Vineet Kwatra1*, Narayan V. Karanth1, Kelum Priyadarshana2,3 and Michail Charakidis1
Abstract
Background: Transplant patients were excluded from the pivotal phase III trials of checkpoint inhibitors in
metastatic melanoma. The efficacy and toxicity profiles of checkpoint inhibitors in this cohort of patients are not
well described. To the best of our knowledge, this is the first case report of a renal transplant patient with stage IV
melanoma treated with a programmed cell death protein 1 checkpoint inhibitor that led to both treatment failure
and renal graft rejection.
Case presentation: We present a case of a 58-year-old white man with a long-standing cadaveric renal transplant
who was diagnosed with a B-Raf Proto-Oncogene, Serine/Threonine Kinase wild-type metastatic melanoma. He was
treated with first-line pembrolizumab but experienced subsequent graft failure and rapid disease progression.
Conclusions: This case highlights the risks associated with the administration of checkpoint inhibitors in patients with
a renal transplant and on immunosuppressive therapy. More specifically, it adds to the literature indicating that,
compared with the cytotoxic T-lymphocyte-associated protein 4 inhibitor ipilimumab, anti-programmed cell death
protein 1 agents are more likely to lead to renal graft failure. Additionally, these novel immunotherapeutics may be
ineffective in transplant patients; therefore, clinicians should be very aware of those risks and carefully consider
selection of agents and full disclosure of the risks to their patients.
Keywords: Melanoma, Checkpoint inhibitors, Transplant, Toxicity, Case report
Background
Programmed cell death protein 1 (PD-1) immune check-
point inhibitors have been shown to significantly im-
prove overall survival among patients with many solid
malignancies, in particular patients with metastatic
melanoma and stage IV small cell and non-small cell
lung cancer [1, 2]. Transplant patients were excluded
from the pivotal phase III trials of immune checkpoint
inhibitors; therefore, the efficacy and toxicity profiles of
these agents in this cohort of patients are not well
described. Furthermore, there is a potential increased risk
of acute graft rejection owing to the activation of T cells
from PD-1 inhibition and risk of cancer treatment failure
due to the concurrent use of immunosuppressive therapy
required to maintain transplant organ function. In this re-
port, we describe a case of a renal transplant patient with
stage IVB-Raf Proto-Oncogene, Serine/Threonine Kinase
(BRAF) wild-type melanoma who was treated with first-
line pembrolizumab (anti-PD-1 agent) that led to subse-
quent graft rejection and rapid disease progression.
Case presentation
A 58-year-old white man received a cadaveric renal
allograft in 2001 for end-stage renal disease secondary to
immunoglobulin M nephropathy. The human leukocyte
antigen (HLA) compatibility of donor to recipient
showed a mismatch of two antigens with peak panel re-
activity antibody of 9%. The patient had been receiving
* Correspondence: vkwatz@gmail.com
1Medical Oncology Department, Alan Walker Cancer Centre, Royal Darwin
Hospital, 105 Rocklands Drive, Tiwi, NT 0810, Australia
Full list of author information is available at the end of the article
© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and
reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to
the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver
(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Kwatra et al. Journal of Medical Case Reports  (2017) 11:73 
DOI 10.1186/s13256-017-1229-z
tacrolimus 1.5 mg twice daily and mycophenolate
mofetil (MMF) 500 mg twice daily over the past 13 years
without any evidence of chronic rejection. The trans-
planted kidney had been functioning well with baseline
serum creatinine <100 μmol/L. The patient’s other
significant comorbidities included hypertension, multiple
resected squamous cell skin cancers, hepatitis C, and
treated latent tuberculosis.
The patient noticed a rapidly enlarging, fungating skin
lesion over the right scapula (Fig. 1a) and complained of
unintentional weight loss of 3 months’ duration. An
excisional biopsy was performed, which showed an
ulcerated nodular melanoma of 21-mm thickness, Clark
level V. The patient’s immunohistochemistry was posi-
tive for homatropine methylbromide 45 (HMB-45),
S100, and melan-A (Fig. 2), and a molecular study
showed wild-type BRAF status. Computed tomography-
based staging revealed multiple liver metastases, an L4
lytic lesion, and left hilar and porta hepatis lymphaden-
opathy. A liver biopsy was performed, which also con-
firmed metastatic melanoma. Tacrolimus and MMF
were stopped. The patient was started on azathioprine
100 mg daily and everolimus 0.5 mg twice daily prior to
commencement of pembrolizumab 2 mg/kg every 3
weeks. The reason for modification of immunosuppres-
sive drugs was to maximize the treatment effect of the
anti-PD-1 inhibitor. Prior to treatment, the patient and
his family were informed about the potential risks of
graft failure and progression of melanoma.
After two cycles of pembrolizumab, the patient’s condi-
tion continued to decline rapidly, with reduced perform-
ance status and an increase in the size of subcutaneous
nodules over his right scapular area (Fig. 1b). His renal
function worsened rapidly with a creatinine level >200
μmol/L (Fig. 3). He declined the options of hemodialysis
Fig. 1 a Fungating melanoma over the right scapula at diagnosis.
b Progressive disease of cutaneous lesions after two cycles
of pembrolizumab
Fig. 2 Malignant melanoma visualized by immunohistochemistry. a High-power view. b Melan-A stain. c S100 stain
Kwatra et al. Journal of Medical Case Reports  (2017) 11:73 Page 2 of 5
and renal biopsy owing to his poor prognosis. His liver en-
zyme and electrolyte levels were within normal ranges,
and his chronic normocytic anemia was unchanged with a
hemoglobin level of 106 g/L. He had mild neutrophilia
(9.6 × 109/L). His C-reactive protein level was 77 mg/L.
He was transferred to a hospice so he could receive best
supportive care, and he died there 3 days later.
Discussion
To the best of our knowledge, this is the first report
describing first-line use of a PD-1 inhibitor in a renal
transplant patient for the management of BRAF wild-type
metastatic melanoma without prior immunotherapy, tar-
geted therapy, or chemotherapy. To the best of our know-
ledge, this is also the first report describing a synchronous
graft rejection and treatment failure with rapid and fatal
Fig. 3 Rise in creatinine in relation to cycle 1 and cycle 2 (C1 and
C2, respectively) of pembrolizumab
Fig. 4 Treatment guideline algorithm for metastatic melanoma. CT Computed tomography, CTLA-4 Cytotoxic T-lymphocyte-associated protein 4,
MET Mesenchymal-epithelial transition factor, MRI Magnetic resonance imaging, PD-1 Programmed cell death protein 1, PET Positron
emission tomography
Kwatra et al. Journal of Medical Case Reports  (2017) 11:73 Page 3 of 5
disease progression. There were two recent published case
reports on PD-1 inhibitors causing renal allograft rejection
[3, 4]. In these two reports, patients had BRAF wild-type
metastatic melanoma managed with a first-line cytotoxic
T-lymphocyte-associated protein 4 (CTLA-4) inhibitor
(ipilimumab) with maintenance of the graft while on ipili-
mumab. After progression, the treatment was switched to
a PD-1 inhibitor, with subsequent graft rejection requiring
hemodialysis. One of the patients was able to achieve dis-
ease control following six cycles of a PD-1 inhibitor. Fur-
thermore, there are two case reports on renal transplant
patients with stage IV melanoma who were treated with
ipilimumab and had good disease response and graft pres-
ervation [5]. A general treatment guideline algorithm for
metastatic melanoma is shown in Fig. 4.
T-cell activation or tolerance to self-antigen depends
on the balance between costimulatory and coinhibitory
signaling [6]. Evidence has shown that the PD-1 and
programmed death-ligand 1 (PD-L1) pathway is impli-
cated in transplant tolerance and prevention of chronic
allograft rejection [7]. In addition, the PD-L1 receptor is
most prominent in renal tubules and highly regulated in
renal transplant recipients. Therefore, it plays an import-
ant role in impairing T-cell response to the transplant
organ [8]. Early data showed that blocking PD-L1, and
not PD-L2, can accelerate graft rejection of a major
histocompatibility complex class II mismatch allograft
[9]. This may explain the currently available data demon-
strating the ability to maintain the allograft when treated
with anti-CTLA-4 inhibitors but rejection of the trans-
planted tissue when treated with anti-PD-1 agents [3, 4].
Tacrolimus is the backbone immunosuppressant for use
in renal transplant patients because it has been shown to be
associated with long-term graft survival [10]. It acts by inhi-
biting T-cell signal transduction. The common perception
in management of transplant recipients with a new diagno-
sis of melanoma is to reduce or change immunosuppres-
sants depending on several factors, including age, HLA
mismatch, and prior history of rejection. Azathioprine and
mammalian target of rapamycin inhibitors are both reason-
able step-down options in long-term recipients when
attempting to maintain graft function [11]. Despite this,
there is inadequate data to help select the most appropriate
immunosuppressant and its interaction with immune
checkpoint inhibitors. Acute allograft dysfunction in this
setting is most likely to be related to acute cell-mediated re-
jection and acute tubular necrosis. Lipson et al. [12] re-
ported a histologically proven case of acute cell-mediated
renal allograft rejection that occurred about 2 months after
administration of PD-L1 inhibitors without the associated
antibodies that participate in rejection. Although their pa-
tient had cutaneous squamous cell carcinoma, a similar
mechanism for transplant rejection can be reasonably as-
sumed in our patient.
Conclusions
Renal transplant patients with stage IV melanoma are
more likely to maintain their graft and have a response if
treated with ipilimumab than if they are treated with
anti-PD-1 agents [5]. PD-1 inhibitors may result in dis-
ease response, but they are more likely to threaten the
transplanted renal tissue with rejection [3, 4]. Therefore,
ipilimumab should be considered as first-line therapy in
renal transplant patients with stage IV melanoma requir-
ing treatment with immunotherapy. As highlighted by
our patient’s case, there is always a risk of graft failure
and disease progression in kidney transplant recipients
on immunosuppressive therapy who are treated with
checkpoint blockade. These patients should be made
aware of this risk.
Acknowledgements
We extend special thanks to Dr. Aijye Lim and the pathology department at
Royal Darwin Hospital for sending us histological images.
Funding
No funding.
Availability of data and materials
The authors agree to discuss and resolve any enquiries from the data and
the material presented in this article.
Authors’ contributions
VK was involved in writing the manuscript. MC was the supervising
oncologist of the case and was involved in final proofreading. KP provided
opinion on the reasons for transplant rejection. NK assisted with the writing
and correction of the manuscript. All authors read and approved the final
manuscript.
Competing interests
The authors declare that they have no competing interests.
Ethics approval and consent to participate
Ethics approval was provided by the Northern Territory Department of Health and
the Menzies School of Health Research (HREC reference number 2016-2631).
Written informed consent for publication could not be obtained from our deceased
patient's next-of-kin despite all reasonable attempts. Every effort has been made to
protect the identity of our patient and there is no reason to believe that our patient
would have objected to publication.
Author details
1Medical Oncology Department, Alan Walker Cancer Centre, Royal Darwin
Hospital, 105 Rocklands Drive, Tiwi, NT 0810, Australia. 2NT Renal Services,
Royal Darwin Hospital, Darwin, NT, Australia. 3Flinders University, Adelaide,
SA, Australia.
Received: 5 September 2016 Accepted: 1 February 2017
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Pembrolizumab for metastatic melanoma in a renal allograft recipient with subsequent graft rejection and treatment response failure: a case report

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