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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5851_Библиотеки_им_академика_М_И_Перельмана.pdf
1 Approach toClinical Reasoning inCritical Care
Table 1.2 Example of a structured review of systems
Organ system Assessment
CNS Brain imaging.
Level of consciousness(LOC).
Evaluation of pain, sedation, and delirium.
Fever (grade, number of spikes, pattern,pulse-temperature relationship).
External ventricular drains/VP shunts, etc.
Penetrating head trauma/skull fracture.
Cardiovascular Vital signs and tissue perfusion (skin, LOC, urine output, etc.).
Electrocardiogram (ECG).
Echocardiogram (ECHO).
Central venous catheters (subclavian, internal jugular, femoral), PICC lines,
chemo port, etc.
Other intravascular devices (e.g., pacemakers, ICDs, LVADs).
Respiratory Chest imaging.
Pattern of breathing.
Ventilation parameters.
Arterial blood gas (ABG).
Color, amount, and characteristics of sputum/endotracheal secretions.
Chest drains/tubes, etc.
Gastrointestinal Abdominal exam/imaging/intra-abdominal pressure (IAP).
Oral/enteral/parenteral feeding.
Bowel movements (frequency, size, consistency).
Stress ulcer prophylaxis (if indicated).
Gastric residuals.
Operative notes.
Abdominal drains, wounds, and stomas.
Genitourinary Urine output.
Inputs–outputs with balance.
IV uids.
Indwelling Foley catheters, nephrostomy catheters, or suprapubic catheters.
Musculoskeletal Bed sores.
Hematomas.
Skin and soft tissue infection.
DVT prophylaxis, etc.
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1.4 Approach toCommon Clinical Presentations intheICU
1.4.1 Sepsis
Septic shock is the commonest cause of circulatory failure in the ICU [7, 15]. Since
common things occur commonly, the diagnostic approach to the patient with circulatory failureshould always consider sepsis as one of the inciting causes. Sepsis
requires a porte d’entree signicant to overwhelm host defense mechanisms [13].
Without a signicant source of infection, sepsis can be safely excluded [12]. Only
few entry sources are implicated in sepsis. The four most common sources of sepsis
in the ICU include pulmonary, gastrointestinal (GI), genitourinary (GU), and intravenous sources [12]. The pharmacist clinician should always assist inlocalizing the
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DECISIONS
Fig.
1.2 Astepwiseapproach
for evaluating
appropriateness of drug
therapy in the ICU
Independent review of systems
(e.g., CNS, CVS/respiratory,
GI/GU, etc.)
Review of patient-specific information
(e.g., initial history, progress notes,
laboratory findings,
medication history, etc.)
Reconcile missing/conflicting
findings with the medical
team
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DRUG THERAPY
source of sepsis. The best approach to the septic patient is to systematically screen
for the potential infection focus in order from most common to least common
(Fig.1.3). Notably, the source of sepsis is almost always a single source. Rarely, if
ever, the septic patient has multiple sources of infection leading to sepsis at the
same time.
Specic clinical and laboratory ndings may aid the diagnosis. Common clinical
signs associated with sepsis include acute encephalopathy, fever, tachypnea, and
tachycardia. Fever is the most recognized sign of infection, dened in the ICU as a
single temperature measurement greater than or equal to 38.3°C [33]. However, not
all causes of fever are of infectious origin. In the ICU, noninfectious causes are
diverse and must be pursued only after careful exclusion of an infectious etiology.
Notably, absence of fever does not rule out infection. Some patients in the ICU are
unable to mount an immune response, characteristic of an ongoing infectious process. Immunocompromising factors leading to a blunted febrile response include
older age, liver/renal disease, use of immunosuppressive agents (e.g., steroids),
solid-organ transplant recipients, and hematological malignancies. In addition to
clinical signs, nonspecic inammatory markers, e.g., WBC, CRP, and ESR, are
typically considered when trying to discern an infectious etiology. However, nonspecicinammatory markers must be interpreted in the proper clinical context as
undue reliance may lead to diagnostic errors. Without a source of infection, elevated
inammatory markers should not prompt initiation of antimicrobial therapy.In the
ICU, the use of inammatory markers, at best, is to complement rather than replace
clinical judgment.
The therapeutic approach to the septic patient depends on the identication of the
likely infection focus [13]. Localizing the site of infection determines the pathogenic ora that needs to be covered with empiric therapy. Antimicrobial therapy is,
1 Approach toClinical Reasoning inCritical Care
Table 1.3 Example of diagnostic approach based on assigning a higher “diagnostic weight” to the
more frequent cause(s)
Clinical ndings/Dx. Most common cause Less common causes
ARDS [6] Infection Aspiration
Hypoglycemia Insulin
NPO status
Hypotension Sepsis (+ source) Hypovolemia
ICU-acquired diarrhea Enteral feeding
Laxatives
Polyuria Excessive uid administration
Diuretics
Noncardiogenic shock
Trauma
Pulmonary contusion
Blood transfusion
Acute pancreatitis
Inhalation injury
Drug overdose
Pulmonary vasculitis
Burn
Drowning
Myxedema coma
Adrenal insufciency
Liver disease
Non-insulin drugs
Cardiogenic cause
Relatively less common causes:
Obstructive cause
Adrenal insufciency
Anaphylaxis
Drug-induced
Myxedema coma
Drug-induced (e.g., tigecycline)
C.Difcile (↑↑↑ watery diarrhea)
Diabetes insipidus
Cerebral salt wasting, etc.
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therefore, appropriate only if based on source localization. Treating a presumed
sepsis without source localization from the outset is the cause of needless, inappropriate therapy. A constellation of clinical signs, when present, can point to the
potential source of infection (Table 1.4). Once the infection focus is discerned,
treatment should be directed at the likely pathogenic ora. Examples of common
pathogenic ora in the lower gastrointestinal tract infections are B fragilis and aerobic gram-negative bacteria, but not Staphylococcus aureus. Conversely,
Staphylococcus aureus are usual pathogens in central line-related infections, but not
B. fragilis [13].Another notable example is Candida spp., which are pathogens in
colonic perforation, butoften nonpathogenic bystanders in pneumonia. The success
of treating sepsis depends on early recognition, source control, and appropriate,
timely antimicrobial therapy.
10
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Fig. 1.3 Astepwiseapproach to screening for the source of sepsis
1 Approach toClinical Reasoning inCritical Care
Table 1.4 Clinical signs commonly associated with each infection focus
Site of infection Referable ndings
Lungs Inltrates +/− fever with purulent secretions, new or
Hepatobiliary (ascending
cholangitis)
Colon Abdominal distention, severe abdominal pain,
Genitourinary Bacteriuria with pyuria plus local or systemic signs of
IV line infection Evidence of infection around the site of insertion (not always
Complicated skin and soft tissue
infections
increased oxygen requirements
Increased liver function tests with cholestatic picture (e.g.,
elevated direct bilirubin)
pneumoperitoneum, etc.
infection
present)
Extreme pain, tenderness, warmth, swelling, redness, etc.
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1.4.2 Acute Encephalopathy
Acute encephalopathy is a global disturbance of brain function, often in the absence
of structural brain disease. Acute confusional state, acute brain dysfunction, acute
brain failure, and altered mental status are non-preferred interchangeable terms
[37]. The underlying mechanism is a pathobiological brain process expressed clinically as an acute change in baselinelevel of consciousness.The cause can be traced
to either intracerebral or extracerebral origin(Table 1.5).The most common etiologies leading to acute encephalopathy may be conveniently divided into: toxicmetabolic, structural/primary CNS processes, and cardiovascular. Toxic-metabolic
encephalopathy is most common, followed by primary CNS processes and cardiovascular conditions. The diagnostic approach to acute encephalopathy depends on
the assessment of all potential causes, a focused history, and a physical examination
to assess for localizing signs.
Toxic-metabolic encephalopathy (TME) is caused by sepsis, hepatic failure,
renal failure, hypoxemia, hypercapnia, hyponatremia, hypoglycemia, hyperosmolar
hyperglycemic state (HHS), hypercalcemia, toxins, drugs, and thiamine deciency.
These factors induce alterations in the normal brain milieu, leading to altered states
of consciousness, going from delirium to coma [14]. Patients with delirium present
with acute uctuating attention, disorganized thinking, and altered arousal but are
awake and responsive. In contrast, patients with coma are in a state of absent consciousness with no response to external stimuli. Although TME is reversible, severe
or sustained insults may lead to neurological sequelae [14]. Identifying and reversing the cause of TME are, therefore, important. Diagnostically, the cause of toxicmetabolic encephalopathy may be evident from the predominant syndromic
signs—e.g., hepatic encephalopathy is the cause of TME in patients with the signs
of decompensated liver cirrhosis including asterixis, ascites,and esophageal varices. Septic encephalopathy is suspected in patients with a source of sepsis (e.g.,
indwelling CVCs) with systemic signs of infection. Although TME is the most
common cause of encephalopathy in the ICU, the clinician should proceed in a
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Table 1.5 Common causes of encephalopathy (“time CNS”)
Toxic Drug overdose or intoxication
Withdrawal
Drug-related causes
Infectious Sepsis
Urinary tract infection (elderly)
Metabolic Electrolyte abnormalities
Endocrine abnormalities
Hepatic encephalopathy
Uremic encephalopathy
Wernicke’s encephalopathy
Hypoxia and hypercarbia
Epileptic Nonconvulsive status epilepticus
Postictal state
Cardiovascular Arrhythmia
Sustained hypotension
Cardiac syncope
Neurodegenerative Alzheimer’s disease
Lewy body dementia
Structural Stroke with mass effect
Thalamic hemorrhage
Traumatic brain injury
Encephalitis
Cerebral vasculitis
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diagnostic workup to rule out a structural/primary CNS-damaging process—if
suspected.
Acute encephalopathy secondary to structural/primary CNS processes is caused,
for example, by severetraumatic brain injury (sTBI),encephalitis/meningoencephalitis, nonconvulsive status epilepticus, stroke in the brainstem, and stroke with
mass effect. Mass lesions or stroke conned to one hemisphere without mass effect,
and without involving the brain stem, will not alter the level of consciousness.It
is rather possible to differentiate structural from toxic-metabolic causes of acute
encephalopathy on the basis of clinical examination [27]. Most notably, ndings
referable to structural damageinclude the presence of localizing signs (e.g., asymmetrical motor signs). The absence of localizing signs suggests alternate causes,
most commonly toxic-metabolic. Specically, toxic-metabolic encephalopathy
causes a uctuating level of consciousness, with an identiable precipitant and
without focal neurological decits [27]. Additionally, involuntary limb movements
(tremors, myoclonus, and asterixis), acid-base disturbances, and abnormalities of
the respiratory patterns (hypoventilation or hyperventilation) are clues to a metabolic etiology[27].
The causes of acute encephalopathy attributable to the cardiovascular system
include hypotension, syncope, and arrhythmia. Notably, syncope causes a drop in
the level of consciousness that is transient, with rapid onset, short duration, and
spontaneous recovery [31]. The cardiovascular causes of syncope include arrhythmia, structural heart disease, pulmonary embolus, acute aortic dissection, and
1 Approach toClinical Reasoning inCritical Care
13
pulmonary hypertension [31]. Syncope due to arrhythmia may not be a straightforward diagnosis. The clinical conundrum in the patient with recurrent, unexplained,
brief episodes of loss of consciousness with spontaneous recovery can be resolved
with the use of a Holter monitor (Fig.1.4). Common cardiac arrhythmias leading to
transient loss of consciousness include ventricular tachycardia, supraventricular
tachycardia, sick sinus syndrome, and atrioventricular (AV) block [31].
1.4.3 Acute Stroke
Stroke encompasses ischemic and hemorrhagic stroke. The vast majority of strokes
are ischemic. Stroke develops instantaneously and usually presents with asymmetric ndings. The absence of localizing signs argues against the diagnosis of acute
stroke. Ischemic stroke is classied according to the underlying etiology into cardioembolic, large-artery atherosclerotic, lacunar small-vessel disease, stroke of
other determined etiology, and stroke of undetermined etiology [1]. The imaging
modality most sensitive for the diagnosis of ischemic stroke is diffusion-weighted
imaging (DWI) [21]. With DWI, the area of infarct appears hyperdense (bright)
(Fig. 1.5). A non-contrast CT of the brain, however, remains the mainstay of
Fig. 1.4 Ambulatory 24-h Holter monitoring reveals episodes of polymorphic ventricular tachycardia [25]
14
Fig. 1.5 A diffusionweighted scan reveals
multiple infarcts (bright) in
more than one territory,
characteristic of a
cardioembolic stroke
Y. Alz a i d i
imaging because of speed, availability, and cost [43]. Unlike DWI, the infarct area
on CT appears hypodense (dark) (Fig.1.6).
Specic ndings on DWI can help identify the source of ischemic stroke
[42].Most notably, a cardioembolic (CE) sourcecauses multiple infarcts in more
than one territory (Fig.1.5). The commonestcause of CE strokes is due to nonvalvular atrial brillation [16, 18, 19].Atrial brillation originates in the atria causing hemostasis, hypercoagulability state, activation of platelets, and the subsequent
thrombus formation. The risk of stroke from atrial brillation depends on specic
factors, assessed using the CHA2DS2-VASc score. The most prominent site for
thrombus formation is in the left atrial appendage, an anatomical structure originating from the main body of the left atrium. The gold standard for the diagnosis/exclusion of a left atrial appendage thrombus is transesophageal echocardiogram (TEE).
In addition to atrial brillation, other ‘high-risk’ causes of CE strokes include left
ventricular thrombus, dilated cardiomyopathy, infective endocarditis,and mechanical prosthetic valve[19]. When ndings are suggestive of a specic subtype of
ischemic stroke, the specic underlying etiology should be investigated.
Hemorrhagic stroke encompasses intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). ICH is caused by hypertension, coagulopathy, and cerebral amyloid angiopathy, a form of angiopathy resulting from the accumulation of
beta-peptide deposits in the walls of blood vessels in the leptomeninges, cerebral
cortex, and cerebellar hemispheres [24]. Hypertension is the most common cause
implicated in more than 50% of detectable hemorrhagic strokes [20, 32]. To some
Approach toClinical Reasoning inCritical Care
1
Fig. 1.6 Axial CT image
of the brain demonstrates,
among other ndings, a
large cortical infarct (dark)
with mass effect (arrow).
Also noted, petechial
hemorrhage within the area
of infarct postthrombolysis. This patient
is likely obtunded
15
extent, the distribution of hemorrhage points to the inciting cause. ICH in the basal
ganglion or thalamic region points to hypertension, while lobar hemorrhage is more
suggestive of cerebral amyloid angiopathy (Fig.1.7). The other less common type
of hemorrhagic stroke is SAH, which causes hemorrhage in the subarachnoid space.
The majority of SAH occurs in the context of aneurysmal rupture. In the setting of
hemorrhagic stroke, a non-contrast-enhanced CT is commonly used. However, CT
angiography is recommended to evaluate for an underlying vascular pathology in
select patient populations [24, 43]. With CT, blood or bone structures (containing
calcium) appear hyperdense (bright) (Figs.1.8 and 1.7).
As previously noted, stroke limited to one hemisphere without mass effect,
excluding stroke in the brainstem, will not affect the level of consciousness. This is
in contrast to stroke with mass effect, stroke in the brainstem, or stroke affecting
multiple territories in both hemispheres (Figs.1.5 and 1.6). ICU management of
patients with acute stroke, in addition to post-thrombolysis care, is centered onneuroprotective measures and prevention of secondary braininjury.
16
Fig. 1.7 Axial CT image
of the brain demonstrates
thalamic hemorrhage
(arrow)
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1.4.4 CNS Infection
CNS infection commonly seen in ICU patients are acute bacterial meningitis and
acute viral encephalitis. TB Meningitis, Neurosyphilis, Toxoplasmosis Encephalitis,
Cryptococcal Meningitis, etc. are less commonly encountered. The mode of pathogenacquisition may be natural or as a result of open head trauma or neurosurgical
procedures. Notably, both immunocompromised and immunocompetent hosts can
acquire CNS infection.A focused history, clinical presentation, cerebrospinal uid
(CSF) prole ndings, CSF PCR, EEG, and radiological features, when combined,
are helpful discriminants for the differential diagnosis.
Acute bacterial meningitis (ABM)is an infectious disease emergencydemanding immediate diagnosis and treatment. The infection starts in the subarachnoid
space and subsequently invades the brain parenchyma leading to severe neurological sequelae [14].This is in contrast to viral meningitis/aseptic meningitis where the
inammation is conned to the subarachnoid space and presents with clear mentation [14].The most common presenting symptoms of ABM include fever, headache,
and nuchal rigidity. Severe headache is a characteristic nding in ABM due to the
presence of nociceptive neurons in the meninges [14]. Other less sensitive meningeal signs referable to ABM include Kernig’s sign (resistance to full extension of