Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5851_Библиотеки_им_академика_М_И_Перельмана.pdf
1 Approach toClinical Reasoning inCritical Care
Fig. 1.8 Axial CT image
of the brain demonstrates
subarachnoid hemorrhage
(SAH). Note the star
shape, characteristic
of SAH
17
the knee) and Brudzinski’s sign (exion of lower limb in response to passive exion
of the neck). Lumbar puncture (LP) ishelpful in establishing the diagnosis, however, it should not delay treatment [38]. Relative contraindications to LP include
increased intracranial pressure, coagulopathy, and suspected spinal epidural
abscesses. A CSF consistent with ABM includes a high opening pressure, a
neutrophil-
predominant pleocytosis (usually WBC count > 1000/microliter), elevated protein concentration, a CSF to serum glucose ratio of less than 0.4, and low
glucose[38].The use of multiplex PCRpanels can rapidly identify the implicated
pathogen, with a special utility in cases where antibiotic administration preceded
the LP. Only limited bacterial pathogens are implicated in ABM. Streptococcus
pneumoniae is the predominant pathogen in community-acquired ABM.In contrast,
hospital-acquired ABM is caused by staphylococcus species and gram-negative
bacilli.
Encephalitis is an inammatory process involving the brain parenchyma with
associated neurologic dysfunction. Neurological ndings, e.g., confusion, personality changes, seizure, focal decits, speech or movement disorders, hemiparesis,
accid paralysis, etc., are characteristic clinical features of encephalitis. An array of
causes including infectious and non-infectious causes have been described. Noninfectious causes include acute disseminated encephalomyelitis (ADEM) and
18
Y. Alz a i d i
anti- NMDA receptor encephalitis, both of which are immune-mediated. The former
is triggered by viral pathogens, including rubella, mumps, varicella, smallpox,
inuenza, and herpes simplex virus (HSV). In contrast, infectious encephalitis is
caused by Herpes simplex virus (HSV), Varicella zoster virus (VZV),
Cytomegalovirus (CMV), Human herpes virus type 6, West Nile virus, Enteroviruses,
etc. The commonest viral cause of encephalitis is due to Herpes simplex virus-1
(HSV-1). HSV-1 has a specic neurotropism.Radiologically, the clue to HSV-1
encephalitis is enhancement of the medial temporal lobe (Fig.1.9). The CSF typical
of HSV-1 encephalitis includes a modest lymphocyte-predominant pleocytosis, an
elevated protein concentration, and a normal glucose. The CSF PCR for HSV is
highly sensitive and specic. Since the CSF is a distant mirror to the infection/
inammation at the brain parenchyma, care should be exercised when excluding
viral encephalitis solely on the basis of negative CSF PCR [35] (Fig. 1.9).
Specically, false negative results may occur early in the disease process or when
the tap is bloody. CMV encephalitis causes a distinct modest neutrophil predominant pleocytosis with periventricular white matter enhancement on T2 weighted
images. CMV encephalitis is almost exclusively seen in immunocompromised
hosts. VZV encephalitis can affect both immunocompromised and immunocompetent hosts and present preceding the rash or after the onset of rash by 6 months.
Early diagnosis and appropriate treatment are critical as delay in diagnosis can
lead to complications and worse outcomes. In the ICU, a febrile patient with penetrating head trauma, post craniotomy/craniectomy, or with internal or external ventricular and lumbar catheters should be suspected to have a CNS infection until
Fig. 1.9 Temporal lobe
enhancement in coronal
T2-weighted MR image.
HSV PCR from
cerebrospinal uid was
negative. PCR was
repeated on a brain biopsy,
which conrmed the
diagnosis of HSV
encephalitis. Source: http://
www.radpod.
org/2007/03/24/
herpes- simplexencephalitis/
1
Approach toClinical Reasoning inCritical Care
19
proven otherwise. In general, treatment starts empirically then directed against a
specic pathogen.
1.4.5 Severe Community-Acquired Pneumonia
Severe community-acquired pneumonia (sCAP) often requires ICU admission and,
in some cases, ventilatory support. The severity of CAP depends on the immune
status of the host and the baseline cardiopulmonary reserve [14]. In other words,
patients with underlying immunocompromised conditions are likely to have a severe
clinical course. Likewise, patients with cardiac or pulmonary dysfunctions at baseline are likely to decompensate following infection with a CAP pathogen. The
pathogens implicated in CAP include bacterial, viral, and fungal pathogens. Specic
clinical, laboratory, and radiological features are combined to discern the etiology of CAP.
Viral causes of CAP include inuenza, SARS-CoV-2, respiratory syncytial virus
(RSV), adenovirus, human metapneumovirus (hMPV), and cytomegalovirus
(CMV). Viral pathogens are differentiated from other nonviral respiratory pathogens by means of imaging, clinical features, and laboratory ndings. Classically,
viral CAP presents on chest imaging as diffuse bilateral interstitial symmetrical
inltrates (Fig.1.10). There are, however, other radiological mimics of viral CAP
that are often missed, including infectious and noninfectious mimics. Noninfectious
mimics of viral CAP include, among others, diffuse alveolar hemorrhage, cryptogenic organizing pneumonia, and drug-induced pneumonitis. Among the infectious
mimics, Pneumocystis jirovecii (PJP) pneumonia is a notorious, nonviral mimic of
viral CAP (Fig.1.11). Laboratory ndings are variably helpful for suspecting a viral
etiology. Inconsistently, thrombocytopenia and lymphocytopenia may accompany
Fig. 1.10 Bilateral diffuse
interstitial inltrates in
keeping with a likely viral
etiology
20
Fig. 1.11 Pneumocystis
jirovecii pneumonia with
LDH >500mg/dL
Y. Alz a i d i
viral CAP; however, neither are sensitive nor specic [34]. Rarely, bacterial pathogens complicate viral CAP, resulting in co-bacterial or secondary bacterial
infections.
Severe community-acquired pneumonia is also caused by fungal pathogens, of
which Pneumocystis jirovecii deserves a special focus. Pneumocystis jirovecii is an
intracellular opportunistic pathogen commonly associated with HIV, but it is a recognized pathogen in other immunocompromised hosts. The clinical presentation is
distinct from viral CAP, in which patients with PJP pneumonia present subacutely
(over several days to weeks) with symptoms of nonproductive cough and progressive exertional dyspnea [2]. Unlike viral CAP, extrapulmonary disease is rare with
PJP pneumonia. Patients presenting to the ICU will typically have severe hypoxemia (PaO2<70mmHg, Aa-gradient >35mmHg). A clinically useful, albeit imperfect, clue to PJP pneumonia is the associatedelevation in serum LDH (>500mg/
dL). The denitive diagnosis is based on histopathologic or cytopathogenic demonstration of the organism with appropriate staining [2]. Notably, bronchoscopy with
bronchoalveolar lavage (BAL) has a lower sensitivity in non-HIV compared to HIV
patients [2]. The diagnosis of PJP pneumonia relies on a high index of suspicion in
the right patient population.
Bacterial CAP in immunocompetent hosts without an underlying cardiopulmonary dysfunction rarely leads to severe presentation mandating ICU care. The usual
patients with severe bacterial CAP are immunocompromised hosts and/or those
with low cardiopulmonary reserve [14]. Both typical and atypical bacteria are
implicated in CAP. The typical respiratory pathogens include Streptococcus pneu-
moniae, Haemophilus inuenzae, and Moraxella catarrhalis. In immunocompromised hosts and chronic alcoholics, Klebsiella pneumoniae is a recognized pathogen
(Fig.1.12). In cystic brosis, Pseudomonas aeruginosa is implicated. Staphylococcus
aureus rarely complicates viral CAP and, if so, presents as cavitary pneumonia [10].
In addition to typical bacterial pathogens, other atypical non-zoonotic pathogens are
causative including Mycoplasma pneumoniae and Chlamydia pneumoniae, and,
rarely, Legionella pneumophila [10]. Specic to atypical CAP are the
Approach toClinical Reasoning inCritical Care
1
Fig. 1.12 Klebsiella
pneumoniae CAP in an
immunocompromised host
Fig. 1.13 Mycoplasma
pneumoniae CAP in a
severely hypoxic patient,
presenting with
extrapulmonary symptoms
21
extrapulmonary manifestations, including gastrointestinal and neurologic symptoms. In fact, atypical CAP can be thought of as a systemic infection involving the
lungs [10]. On chest imaging, bacterial CAP presents as alveolar airspace opacities
with air bronchograms, thus differentiating bacterial CAP from viral CAP
(Fig.1.13).
22
Y. Alz a i d i
1.4.6 Nosocomial Pneumonia
Nosocomial pneumonia (NP) including hospital-acquired pneumonia (HAP) and
ventilator-associated pneumonia (VAP) is common in the ICU.The organisms most
responsible for NPs are aerobic gram-negative bacilli. The clinical signs of pneumonia include increased colored secretions, pulmonaryinltrates, tachypnea, and new
or increased oxygen requirements. The mere recovery of a pathogen without the
accompanied clinical signs of infection should not prompt initiation of antibiotics.
Radiological ndings of bacterial NPtypically include lobar or multilobar airspace
alveolar opacities/consolidation with air bronchograms.
NP is usually caused by a single pathogen. Recovery of multiple organisms from
the sputum/endotracheal aspirate is likely to represent colonization. The organismstypically implicated in NP are Klebsiella pneumoniae, Pseudomonas aerugi-
nosa, and, less frequently, Acinetobacter baumannii. Pseudomonas aeruginosa
commonly colonizes secretions of ventilated patients, and unless
accompanied by characteristic ndings, it should not be treated [14] (Fig.1.14).
Notably,Staphylococcus aureus is not a typical cause of NP [14]. In the setting of
community-acquired pneumonia, Staphylococcus aureus rarely causes infection
following viral pneumonia. The negative nasal MRSA PCReffectively rules out
MRSA as a causative pathogen in suspected pneumonia.Not uncommonly, mechanically ventilated patients may develop ventilator-associated tracheobronchitis
(VAT), which presents with clinical signs of pneumonia but without radiological
evidence of infection. Importantly, when evaluating patients suspected of VAT,
Fig. 1.14 Chest
radiograph of nosocomial
pneumonia caused by
Pseudomonas aeruginosa.
Note the cavitary lesion
(arrow), hallmark of
infection with
Pseudomonas aeruginosa
Approach toClinical Reasoning inCritical Care
1
23
other causes should be excluded including VAP which may not be apparent in portable chest radiographs (Fig.1.15).
Herpes simplex virus (HSV) rarely causes nosocomial pneumonia in ventilated
patients. HSV may be suspected as the cause of non-resolving VAP, manifestingclinically as failure to wean from the ventilator or, more typically, assevere
hypoxemiarequiring ahigh FiO2 [17]. Importantly, reactivation of HSV is common
in mechanically ventilated patients and should be distinguished from true HSV
pneumonia [30]. The mere detection of HSV from respiratory samples does not
prove its etiologic role. The denitive diagnosis of HSV pneumonia is made with
cytopathological evidence of invasion. In addition to HSV, other common respiratory viruses can be transmitted from healthcare staff to patients, especially during
viral seasons, leading to nosocomial pneumonia.
1.4.7 Pulmonary Edema
Pulmonary edema develops secondary to cardiogenic and noncardiogenic causes,
with cardiogenic pulmonary edema being the most common cause. Knowledge of
the cause of pulmonary edema has important implications for management [41].
The differentiation of cardiogenic versus noncardiogenic pulmonary edema combines ndings from history, clinical investigations, and, to some extent, radiological
features. Substantial overlap between cardiogenic and noncardiogenic pulmonary
edema, however, remains.
Fig. 1.15 A normal supine
chest radiograph. The
patient had purulent
secretions with fever in
keeping with VAT. What
not to overlook is the
central venous catheter
(arrow), another potential
source of fever
24
Y. Alz a i d i
Cardiogenic pulmonary edema is caused by cardiac-related etiologies, most
commonly seen in the setting of heart failure.The mechanism underlying cardiogenic pulmonary edema is increased pulmonary capillary pressure, transuding uids rst into the interstitium and later into the alveolar space [41]. Signs of interstitial
edema include a centrally located, buttery pattern of linear and reticular opacities.
If progressed, a conuent airspace consolidation ensues, reecting uid accumulation in the alveolar space. These radiological ndings, however, are common in both
cardiogenic and noncardiogenic pulmonary edema. Associated ndings that are
characteristic, but not specic, for cardiogenic pulmonary edema include cardiomegaly with bilateral pleural effusions, more prominent in the right pleural cavity
(Fig.1.16). Notably, rapid regression of congestive signs with effective uid removal
and restoration of compensated state favors cardiogenic pulmonary edema.
Noncardiogenic pulmonary edema is caused by a multitude of factors, with acute
respiratory distress syndrome (ARDS) being the most important cause in terms of
severity. The mechanism underlying pulmonary edema in ARDS is increased
alveolar- capillary permeability, leading to the inux of protein-rich uids into airspaces [40, 41].ARDS iscaused by either pulmonary or extrapulmonary factors.
Direct pulmonary insultsinclude pneumonia, aspiration, radiation, inhaled toxins,
and thoracic trauma. Extrapulmonary factorsby contrast include sepsis, acute pancreatitis, burn, non-thoracic trauma, and blood transfusions. Certain features differentiateARDS from that of cardiogenic pulmonary edema and include a known
insult within 1week of onset, noncardiogenic bilateral opacities on chest imaging,
and refractory arterial hypoxemia [40] (Fig.1.17).
Fig. 1.16 Chest
radiograph of cardiogenic
pulmonary edema. Note
the increased cardiac
shadow with bilateral
pleural effusions, more
prominent in the
rightpleural cavity (arrow)
1 Approach toClinical Reasoning inCritical Care
Fig. 1.17 Chest
radiograph of
noncardiogenic pulmonary
edema. This patient had
CMV pneumonitis with
refractory arterial
hypoxemia
25
1.4.8 Fever
Fever (≥38.3°C) is common in ICU patients. The search for the cause of fever can
be difcult, even for the experienced clinician. The approach to fever in the ICU is
based on diagnostically discerning infectious from noninfectious fevers. In general,
fever in a patient with a source of infection is an “infectious fever” until proven
otherwise. This approach emphasizes the critical importance of early diagnosis and
should not prompt initiation of antimicrobial therapy in otherwise stable patients
unless an infectious cause is discerned. Notably, the source of infection can be overt
or, in some cases, hidden. Hidden, or less apparent, infectious causes of fever
include surgical site infections, acute acalculous cholecystitis, septic thrombophlebitis, intra-abdominal abscess collection, C. difcile colitis, sinusitis, and others.
Each of these causes should be suspected in the right clinical context; for example,
intra-abdominal abscess is suspected in patients with known risk factors, including
a recent history of abdominal surgery, and acute acalculous cholecystitis presents
with leukocytosis and abnormal liver tests. When all possibilities of an infectious
etiology have been exhausted, a noninfectious cause should then be entertained.
Fever of noninfectious origin in the ICU is caused by deep venous thrombosis, pulmonary embolism, myocardial infarction, central fevers, relative adrenal insufciency, acute pancreatitis, gastrointestinal hemorrhage, atelectasis, transfusion of
blood products, vasculitis, cryptogenic organizing pneumonia, and drugs [33].
Drug fever stands out as a unique cause of noninfectious fever withdiscernible
clinical features. The pattern of drug fever is continuous or intermittent, usually
high grade, and closely resembles fever of infectious origin. All too often, the diagnosis is made after a lack of response to the indiscriminate use of antimicrobial
therapy. The associated clinical ndings in drug fever reect the likely underlying
26
Y. Alz a i d i
hypersensitivity reaction and include mild-to-moderate transaminitis, leukocytosis,
eosinophilia, and elevated erythrocyte sedimentation rate (ESR) [11]. Important
diagnostically, patients with drug fever will not appear in distress [11]. Skin rash
may or may not accompany drug fever. However, the presence of a skin rash, per se,
does not prove drug fever. It is common for clinicians to ascribe skin rash to drugs
alone. Other febrile illnesses encountered in the ICU may present with skin manifestations, including various infectious diseases. Important of all, drug fever is a
diagnosis of exclusion. If drug fever is suspected, the medication list should be
scrutinized for potential culprits. The most common causes of drug fever are antimicrobial and antiepileptic agents. Once the inciting drug is discontinued, a rapid
defervescence occurs, usually within 72h.
References
1. Adams HP Jr, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, Marsh EE 3rd.
Classication of subtype of acute ischemic stroke. Denitions for use in a multicenter clinical
trial. TOAST.Trial of Org 10172in Acute Stroke Treatment. Stroke. 1993;24(1):35–41.
AIDSinfo,
2.
adults and adolescents with HIV. 2019.
Arono
3.
clinical reasoning. J Gen Intern Med. 2019 Sep;15(34):1941–5.
Auerbach
4.
Harris A, Flynn E, Schnipper JL.Diagnostic errors in hospitalized adults who died or were
transferred to intensive care. JAMA Intern Med. 2024;184(2):164–73.
Ball JR, Miller BT
5.
National Academies Press (US); 2015.
6. Bellani G, Laffey JG, Pham T, Fan E, Brochard L, Esteban A, Gattinoni L, Van Haren F,
Larsson A, McAuley DF, Ranieri M. Epidemiology, patterns of care, and mortality for
patients with acute respiratory distress syndrome in intensive care units in 50 countries.
JAMA. 2016;315(8):788–800.
Cecconi M, De Back
7.
Pinsky MR, Teboul JL, Vincent JL.Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Med.
2014;40:1795–815.
Crosk
8.
N Engl J Med. 2013;368(26):2445–8.
Crosk
9.
asing. BMJ Qual Saf. 2013;22(Suppl 2):ii58–64.
10. Cunha BA.Community-acquired pneumonia: diagnostic and therapeutic approach. Med Clin
North Am. 2001;85(1):43–77.
11. Cunha BA. Antibiotic selection in the penicillin-allergic patient. Med Clin North Am.
2006;90(6):1257–64.
Cunha B
12.
Cunha
13.
2008;24(2):313–34.
Cunha CB, Cunha B
14.
care medicine. CRC Press; 2020 Jul 12.
Access. Guidelines for the prevention and treatment of opportunistic infections in
witz PB, Williams DM, Henderson MC, Winston LG.Mind the base rate: an exercise in
AD, Lee TM, Hubbard CC, Ranji SR, Raffel K, Valdes G, Boscardin J, Dalal AK,
, Balogh EP, editors. Improving diagnosis in health care. Washington, DC:
er D, Antonelli M, Beale R, Bakker J, Hofer C, Jaeschke R, Mebazaa A,
erry P.From mindless to mindful practice—cognitive bias and clinical decision making.
erry P, Singhal G, Mamede S.Cognitive debiasing 1: origins of bias and theory of debi-
A.Infectious diseases in critical care medicine, vol. 27; 2007. p.590.
BA.Sepsis and septic shock: selection of empiric antimicrobial therapy. Crit Care Clin.
A, editors. Infectious diseases and antimicrobial stewardship in critical