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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3080_Библиотеки_им_академика_М_И_Перельмана
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The Patient with Chest Pain and a Rash
219
With this new information, will you add any
diagnoses to your original list of differentials?
Opportunistic infections dening development of acquired immunode-
ciency syndrome (AIDS)
Most opportunistic infections occur with CD4
+
count <200 cells/μL.
If Sudip has oesophageal candidiasis rather than simply oral,
this is categorised as an opportunistic infection. Investigate for
candida involvement of the trachea, bronchi and more distal
respiratory tracts.
Other opportunistic infections include the following.
Coccidioidomycosis(‘valley fever’ pneumonia)
Cryptococcus neoformans(particularly in lung and brain tissue)
Cryptosporidium (usually causing diarrhoea)
Cytomegalovirus (brain, eye, gut and respiratory involvement)
Herpes simplex(multisystemic)
Histoplasma capsulatum(pneumonia)
Mycobacterium(multisystem disease, especially pneumonia)
Pneumocystisjirovecii(particularly causing pneumonia; previ-
ously Pneumocystis cariniior PCP)
Toxoplasma gondii(particularly lung and brain involvement)
Salmonella
Immune reconstitution inammatory syndrome (IRIS)
This is a worsening of symptoms following the initiation of anti-
retroviral treatment (ART). There is restored immunity to a range
of infective and non- infective elements.Presentation varies bet-
ween individuals. The incidence of IRIS is unknown but may be up
to 25%. Risk factors include male sex, young age, lower CD4
+
count
and higher viral RNA load.
Diagnostic criteria for IRIS (French etal., AIDS, 2004).
Major criteria– opportunistic infections in patients responding
to antiretroviral drugs, decrease in plasma HIV RNA by at least
1log
10
copies/mL.
normally independent, he works in a bank and does not see the doctor for
anything in particular. He has been drinking more alcohol lately as work
has been stressful but no more than 2–3 glasses of wine in the evening. He
has not travelled anywhere recently.
You thank the family for their time and, shortly after you leave the room,
Ben comes to nd you to speak condentially. He informs you that Sudip
is undergoing treatment for HIV. Following Sudip’s divorce, he started a
relationship with Ben. All the family, except Sudip’s mother, are aware of
this and are supportive. Sudip, however, does not want his mother to know
that he is in a relationship with a man. None of the family are aware that
Sudip is HIV positive and he does not want them to know. Sudip recently
started taking antiretroviral drugs. Ben knows nothing more about the HIV
treatment as Sudip is a very private man. Ben is HIV negative.
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Clinical Cases in Critical Care
220
Minor criteria– increased CD4
+
T- cell count after ART, increase
in immune response to relevant pathogen or ‘delayed-
type
hypersensitivity’, spontaneous resolution of disease without
specific treatment and with continuation of antiretrovi-
ral therapy.
Sudip's confusion may be explained by HIV or AIDS
HIV- related encephalopathy orprogressive multifocal leucoencepha-
lopathy(PML).Although most
adults have been exposed to JC (John
Cunningham) virus,most do not experience problems. In patients
with HIV, JC virus infects oligodendrocytes and leads to widespread
demyelination in the central nervous system,causing PML.
Lymphoma– can develop during HIV stage 3. This may explain the
lymphadenopathy.
Kaposi sarcoma– Sudip's lesions would be consistent with Kaposi sar-
coma. This manifestation of infection with human herpes virus 8would
be consistent with a diagnosis of AIDS.
Mycobacterium tuberculosis (TB)
TB is the most common pathogen seen in association with IRIS.
Presentation often involves fever, respiratory failure and lymph-
adenopathy.
HIV patients are particularly vulnerable to multidrug- resistant
TB (MDR- TB). Extensively drug- resistant TB (XDR- TB) has been
described in HIV- positive patients and has an extremely high
mortality.
Consider moving Sudip to a side room if he is not already in one and
use an FFP3mask when performing aerosolising procedures until
TB has been ruled out.
How does this information affect your
investigations?
Background information is needed regarding Sudip's diagnosis and treatment.
When was he diagnosed, when did he start treatment, what treatment did he
start? Review relevant clinic letters. Discuss his case with specialists in HIV
management, microbiology and infection control.
Request the following additional investigations:
CD4
+
count and CD8
+
count.
RNA viral load.
Galactomannan and beta- D- glucan to look for invasive fungal infection.
Serumlactate dehydrogenase (LDH).
Bronchoscopic washings for MC&S.
If a family member wants to know Sudip’s HIV
status, what can you tell them?
Ben has stated that Sudip does not want his family to know his HIV status. There
is no information to suggest that his family are at risk of having contracted
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The Patient with Chest Pain and a Rash
221
HIV from him. In the UK, the risk of harm to others must be serious enough
to outweigh breaching the patient's right to condentiality– that does not
appear to be the case here. If in doubt, consult your hospital legal team and
your medical protection society.
What is HIV?
HIV is a type of lentivirus. This cytopathic retrovirus is known to have two
types: HIV-
1 (majority of cases) and HIV- 2 (usually a milder course and
mostly seen in mother-
to- child transmission in West Africa). The retrovirus
uses reverse transcriptase to transcribe viral RNA into host DNA. CD4
+
cells,
T-
helper cells, are preferentially infected and produce multiple copies of the
HIV virus. Eventually this leads to the premature death of the host cell. There
is a marked drop in the CD4
+
count, leaving the patient susceptible to infec-
tion and malignancy.
Primary HIV begins when HIV rst enters the body. The HIV life cycle
involves six phases:
1.
Binding and entry
2. Reverse transcription
3.
Integration
4. Replication
5. Budding
6. Maturation
Unchecked, the infection normally progresses through four phases– sero-
conversion illness, an asymptomatic stage, a symptomatic stage and nally
late- stage HIV and AIDS.
The World Health Organization (WHO) classies infection as follows:
Stage 1 (HIV infection)– CD4
+
count at least 500 cells/μL
Stage 2 (HIV infection)– CD4
+
count 350–499 cells/μL
Stage 3 (advanced HIV disease, AHD)– CD4
+
count 200–349 cells/μL
Stage 4 (AIDS)– CD4
+
count <200 cells/μL
According to UNAIDS/WHO, in 2020 there were approximately 37.7 mil-
lion people worldwide living with HIV/AIDS. The vast majority of those are
in low- or middle- income countries.
What drug treatments are available for HIV?
Nucleoside analogue reverse transcriptase inhibitors (NRTI),e.g.zido-
vudine, lamivudine, abacavir
Non- nucleoside reverse transcriptase inhibitors (NNRTI),e.g.nevirapine
andrilpivirine
Protease inhibitors (PI),e.g.darunavir, ritonavir and indinavir
Integrase inhibitors,e.g.raltegravirand elvitegravir
Fusion inhibitors,e.g.maraviroc and enfuvirtide
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Clinical Cases in Critical Care
222
HAART (highly active ART) or cART (combination ART) is a combination
of these drugs designed to decrease viral load and promote the patient's natural
immune system. Often the combination will be two NRTIs plus a PI.
Adverse eects from these drugs can be multiple and include neuropathy,
myopathy and hepatotoxicity. Ritonavir is a potent cytochrome p450inhibitor
so care must be taken to review polypharmacy and avoid potentially cata-
strophic drug interactions.
Cabotegravir and rilpivirine can now be delivered via injection every
2
months to qualifying patients.
How do you interpret the CD4
+
/CD8
+
ratio and viral
load results?
An immunocompetent patient should have a CD4
+
/CD8
+
ratio greater than 1.0
(normally >1.5). In chronic HIV infection, increasing numbers of CD8
+
cells
with depletion of CD4
+
cells result in a falling ratio. Sudip's ratio is extremely
low, suggesting immunocompromise.
A CD4
+
count below 200 cells/μL leaves a patient vulnerable to opportu-
nistic infections.
A viral load of 5.3log
10
equates to approximately 200 000 copies/mL. A high
viral load is generally considered to be greater than 100 000 copies/mL (approx-
imately 5log
10
). Undetectably low viral load is less than 20 copies/mL (approx-
imately 1.3log
10
).
What treatments are available for TB?
First- line drugs are rifampicin, isoniazid (often given in combination
with rifampicin as Rinah
®
), pyrazinamide and ethambutol. A standard
course of treatment is all four drugs for 2 months then Rinah for a
further 4 months.
Second- line drugs include streptomycin, levooxacin, moxioxacin, line-
zolid, carbapenems with clavulanic acid, andcycloserine.
Regular visual eld testing is required with ethambutol, which can limit
its use in critical care.
The CT head reports no abnormality found. The CTPA does not show
pulmonary embolus and rules out a pneumothorax. There are widespread
pulmonary inltrates, mediastinal lymphadenopathy and pleural eusions.
You get in touch with the HIV specialist centre and nd that Sudip was
diagnosed with HIV 4
weeks ago. He started ART 3 weeks ago and was also
being treated for TB.
Your investigations reveal CD4
+
count 37 cells/μL, CD8
+
count 321 cells/μL,
CD4
+
/CD8
+
ratio is 0.12, HIV RNA 5.3log
10
viral load.
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The Patient with Chest Pain and a Rash
223
What antifungal drugs are available and how do
they work?
See Figure17.1.
Azoles– inhibit the conversion of lanosterol to ergosterol, an integral
component of fungal cell membranes. These are the triazoles (e.g. uco-
nazole, itraconazole, voriconazole) and imidazoles (e.g. ketoconazole).
Echinocandins– e.g. caspofungin, anidulafungin, micafungin. They
inhibit 1,3- beta- D- glucan synthase. Beta- glucan is essential for produc-
tion of the cell wall.
Polyenes– such as amphotericin B and nystatin. These bind to ergosterol
and increase the permeability of cells, leading to cell death.
Allylamines– such as terbinane. These inhibit squalene epoxidase
which converts squalene to ergosterol. Squalene, toxic to fungal cells,
accumulates and causes cell death.
Nucleoside analogues– for example, ucytosine. This pyrimidine ana-
logue is converted into 5- FU in fungal cells. Through various mecha-
nisms, this inhibits fungal DNA synthesis.
Squalene
Lanosterol
Ergosterol
Ergosterol-rich fungal
cell membrane
Echinocandins
Beta-glucan rich
fungal cell wall
Terbinafine
Azoles
Flucytosine
Polyenes
Figure 17.1: Mechanisms of actions of antifungal drugs.
Source: Theophilus Samuels.
You discuss the case with the HIV specialist doctor who thinks this is IRIS.
After discussing the risks and benets, you decide to start high-
dose steroids.
She recommends you treat for Pneumocystis jirovecii – you commence high-
dose co- trimoxazole. After discussion with your resident microbiologist, you
also decide to add an antifungal agent.
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Clinical Cases in Critical Care
224
What is the mortality for patients with HIV?
The Antiretroviral Cohort Collaboration published an article in the Lancet
in 2017which showed that survival rates are improving, possibly through a
combination of less toxic antiretroviral drugs, better adherence and better
management of co-
morbidities.
Prognosis continues to improve for those treated early in the course of their
disease. Young people in Europe and the developed world who survive the rst
year of ART are now likely to have near normal life expectancy.
The mortality associated with IRIS is not clearly documented but with mild
IRIS, it is extremely low. ART should generally be continued throughout illness
except in life-
threatening situations.
Further reading
Ghosn, J., Taiwo, B., Seedat, S. etal. (2018). HIV. Lancet 392: 685–697. Excellent of
overview of HIV, particularly with regard to medications.
Barbier, F., Mer, M., Szychowiak, P. etal. (2020). Management of HIV infected
patients in the intensive care unit. Intensive Care Med. 46 (2): 329–342. Informative
review article on HIV in critical care.
Ritter, J., Flower, R., Henderson, G. etal. (2020). Pharmacology. St Louis: Elsevier.
Authoritative textbook on pharmacology.
Sudip continues to deteriorate over the next 24 hours with worsening gas
exchange and renal impairment. You insert bilateral chest drains, com-
mence renal replacement therapy and place him into the prone position.
Two further prone positioning sessions are repeated for 16
hours each and
Sudip's condition eventually begins to improve. Following discussion with
the HIV specialist, you briey withhold ART while Sudip's condition is pre-
carious. By day 3, he begins to improve.
Sudip is successfully extubated on day 9. Moved by the experience of nearly
losing him, Ben proposes marriage to Sudip on day 10. Sudip accepts. He is
discharged to the ward on day 11.
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Clinical Cases in Critical Care, First Edition. Alice Myers and Theophilus Samuels.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Describe Figure 18.1. What is the diagnosis?
This is an ECG rhythm strip showing a polymorphic ventricular tachycardia,
i.e. torsades de pointes.
What are the adverse features of arrhythmias?
According to the Resuscitation Council UK, these are as follows:
Shock
Syncope
Myocardial ischaemia
Cardiac failure
How do you proceed?
The patient has developed torsades de pointes and is cardiovascularly unstable.
Follow the Resuscitation Council Advanced Life Support Guidelines (2021),
taking an ABDCE approach.
18
The Young Patient
Who Collapses
Y
ou attend the resuscitation department following a medical emergency call.
An 18-
year- old woman has been brought in by ambulance following a col-
lapse at home. Her parents tell you that she ‘blacked out’ after going running.
By the time the ambulance arrived at her home, she had roused. Now, in the
ED, she is found to have uctuating consciousness, at worst GCS 8 (E1V2M5),
BP82/43
mmHg, HR 184 bpm, RR 10 breaths per minute, oxygen saturations
93% on air. She does not appear to have lost cardiac output at any time.
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Clinical Cases in Critical Care
226
Administer oxygen, protecting the airway if required.
Obtain intravenous access, send bloods and a blood gas (paying attention
to electrolytes and glucose).
Ensure full monitoring.
Give magnesium 2 g over 10 minutes as the specic treatment for tor-
sades de pointes.
What could be the underlying cause of Belle’s
arrhythmia?
1. Congenital– Belle is only 18 years old. This could represent the rst pre-
sentation of a congenital cardiac disorder.
Inherited channelopathy– congenital long QT syndromes include
Jervell Lange–Neilsen (associated with deafness) and Romano–
Ward. Brugada syndrome may first present as sudden cardiac
death in a young person and the arrhythmia produced can
resemble torsades.
Structural defect– although it is less likely than many of the acquired
causes, it is possible she could have an undiagnosed congenital
anomaly such as hypertrophic obstructive cardiomyopathy (HOCM),
or valvular or septal defect.
2.
Acquired
Electrolyte imbalance– possibly secondary to malabsorption, drug
use, metabolic disorders, or eating disorders.
Thyroid disease.
Sepsis.
Drug toxicity– prescription or illicit.
Coronary artery disease– the most common cause of polymorphic
ventricular tachycardia in adults is coronary artery disease. Myocar-
dial infarction (MI), hypertension and acquired valvular defects, while
not impossible, are less likely in this young patient.
Figure 18.1: ECG rhythm strip
You treat the arrhythmia successfully and the young woman, Belle, stabilises
and regains consciousness. You are now able to assess her fully. Belle looks
extremely thin. She remains quiet and minimally communicative, saying
only that she is cold and wants some water. Her BP is now 90/52
mmHg, HR
125 bpm, RR 22 breaths per minute. She appears dehydrated with poor skin
turgor and central capillary rell time of 5 seconds. She has bibasal crepita-
tions on auscultation of the lung elds.
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The Young Patient Who Collapses
227
What are your immediate concerns?
Cardiac status– she has presented with a malignant arrhythmia and has
signs which could be consistent with cardiac failure.
Nutritional status.
Which key aspects of Belle’s medical history do you
want to know?
Ideally, obtain a history from Belle herself. However, if she is unwilling or unable
to communicate, obtain a collateral history from her GP, family or friends.
Medical notes from any previous admissions should be reviewed for the
following:
Symptoms suggesting cardiac pathology, e.g. fainting, blackouts, seizures
or palpitations.
Symptoms of underlying gastrointestinal disease.
Past medical history of deafness.
Family history of long QT syndrome or sudden cardiac death.
Psychiatric history– in light of a possible eating disorder.
Drug history– prescribed, over the counter and illicit.
What investigations do you need?
Bedside tests
12- lead ECG– look for evidence of long QTc interval.
Pregnancy test – amenorrhoea and collapse in a young woman of
child- bearing age could represent ruptured ectopic pregnancy.
Blood tests
Arterial blood gas– gas exchange may be impaired due to cardiac failure.
Metabolic acidosis may have developed due to dehydration and kidney
or liver injury. Metabolic alkalosis could have developed due to hypoka-
laemia. Assess lactate, base decit and electrolytes.
FBC– malnourishment may lead to anaemia or neutropenia and sepsis
could be indicated by raised WBC.
U&E– with malnutrition, it is necessary to measure sodium, potassium,
calcium, phosphate and magnesium levels. Review urea and creatinine
as Belle is dehydrated.
LFTs– important to review for nutritional status and drug history.
Glucose and ketones.
Thyroid function tests – thyroid disease can cause arrhythmias and
changes in weight. In addition, hypothyroidism may develop because
of starvation.
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Clinical Cases in Critical Care
228
Belle's parents tell you that she dropped out of university 2 months ago and
has been withdrawn, refusing to eat and exercising excessively. They tried
encouraging her to seek help but she refused. There is no family history of
cardiac disorders. Belle has always been t (a keen dancer) and is not known
to take drugs or drink alcohol. She has never been seen by a psychiatrist
although her parents note that the nurse at her secondary school did suggest
she should see someone for counselling.
The arterial blood gas (on 3
L/min O
2
via nasal cannulae) reveals pH 7.30,
PaO
2
8.1 kPa, PaCO
2
3.2 kPa, base excess –6.7 mmol/L, Na 134 mmol/L, K
2.3
mmol/L, HCO
3
17 mmol/L, Cl 101 mmol/L, lactate 3.4 mmol/L. Urine
dip is positive for blood and strongly positive for ketones.
The initial blood tests reveal Hb 114
g/L, WBC 3.9 × 10
9
/L, plats 117×10
9
/L,
urea 8 mmol/L, creatinine 125 μmol/L, magnesium 0.5 mmol/L, phosphate
0.3 mmol/L, Ca 0.98 mmol/L, ALP93 U/L, bilirubin 6 μmol/L. Blood ketones
are high. CRP result is pending. ECG demonstrates long QTc interval.
Focused ultrasonography demonstrates a small hyperdynamic left ven-
tricle, with visual evidence of hypertrophy. No signicant valvular regurgitant
lesions are seen. Lung US demonstrates multiple bilateral B- lines throughout.
Imaging
Chest radiograph.
Echocardiogram.
What is Belle’s anion gap?
Anion gap Na K Cl HCO
3
Belle’s anion gap is (134 + 2.3) − (101 + 17)=18.3 mmol/L. The normal anion
gap is between 4 and 12 mmol/L. A raised anion gap suggests the presence of
unmeasured anions. Note, that even with omitting K
+
(see Case 4), the anion
gap is still above normal.
What are the most likely causes of Belle’s raised
anion gap?
The main causes to remember are lactate, ketones, toxins and renal failure
(see Case 4).
In Belle’s case, she may have taken an overdose so it would be appro-
priate to add paracetamol and salicylate levels to her blood tests and a toxi-
cology screen.
Belle’s raised anion gap is most likely to be due to ketosis.
Patients with eating disorders can present with dierent patterns in acid–
base derangement. Metabolic alkalosis is common secondary to vomiting or
diuretic misuse. Acidosis can arise following laxative misuse. Belle’s case is
complicated through presentation with cardiovascular instability and renal
impairment.
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