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_2721_Библиотеки_им_академика_М_И_Перельмана
.pdf
severity of pneumonia. CURB uses four clinical
parameters to assess the severity of pneumonia:
confusion, urea concentration greater than
7 mmol/L, respiratory rate greater than 30 breaths
per minute and low blood pressure. Two or more
of these criteria indicate an increased risk of
death.
1
CURB 65 takes age greater than or equal
to 65 years old into account as well as the other
CURB criteria.
12
The PSI uses 20 demographic, clinical, and
laboratory criteria to determine the severity of
pneumonia. The PSI rule was derived and validated as part of the pneumonia patient outcomes
research team (PORT), which prospectively studied 14,199 adults to determine which patients
were at low risk of death.
14
These criteria are used
to categorize patients into five classes of increasing risk of death.
1,14
Other indexes include the shock index (SI:
pulse rate divided by the systolic blood pressure).
The adjusted shock index (ASI) is the same as SI
but uses a pulse rate adjusted for temperature by
decreasing the pulse rate by 10 for each 1 degree
C above 37 degrees C. There is the confusion, age,
respiratory rate, shock index (CARSI); CARASI is
the same as CARSI but uses the adjusted shock
index.
13,15
Patients deemed well enough to go home
should have antibiotics initiated in the ED prior
to discharge. Patients who require intubation or
pharmacologic blood pressure support should be
admitted to the ICU.
Patients admitted to the medical floor are
assessed as being too ill to go home or to the observation unit (OU). These patients usually may demonstrate several of the risk factors for pneumonia
(Table 29.1) or medical conditions that are associated with subsequentadmission to the hospital after
an OU stay (Table 29.2). In some cases it will be the
clinical judgment of the emergency physician that
warrants admission. In other cases it will be the
social environment into which the patient is being
discharged that will mandate hospitalization until
the social situation can be improved.
Patients admitted to the OU should be expected
to be improved within 24 hours or within the time
parameters of your OU. Inclusion and exclusion
criteria for OU referral are listed in Table 29.3.
Patients should not be placed into the OU if they
require emergent intubation or pharmacologic
blood pressure support, or have a markedly abnormal vital sign, new hypoxia, and/or ECG changes
consistent with an acute coronary syndrome.
Observation Unit Management
Antibiotic treatment should be initiated in the ED
or soon after admission to the OU. There are
various treatment regimes. Generally parenteral
treatment regime should be initiated in the ED
and continued in the OU with transition to the
outpatient regime at the time of discharge. If the
patient has not improved enough for discharge,
the patient will be admitted. Signs that a patient is
ready for discharge include: decreased general
malaise or weakness, less shortness of breath,
decreased cough, decreased fever, and an overall
improved sense of well-being. Signs that a patient
Table 29.2 Factors Associated with Subsequent
Hospitalization after an Observation Unit Stay
Tuberculosis
Alcoholism
Chronic debilitation
Comorbid illness
Osteoporosis
Persistent symptoms
Persistent fever
Adapted from Chan et al.
16
Table 29.1 Risk Factors for Development of Pneumonia
Diabetes
Stroke
COPD
Congestive heart failure
End stage renal disease
Liver disease
Muscular dystrophy
Chest wall deformity
Various feeding tubes
Seizure disorder
Chronic alcoholism
Illicit drug use
Elderly
Immunosuppression
Community Acquired Pneumonia
032
20:58:53
is not well enough for discharge include: worsening
of the presenting symptoms or exacerbation of
chronic underlying conditions (diabetes, CHF,
COPD). The development of hypoxia or hypotension or worsening general weakness are signs that
the patient is not yet well enough to go home.
Some elderly or debilitated patients may be slightly
improved but may not be well enough to go home
and resume their activities of daily living (feeding,
ambulation, personal hygiene, etc.). A study by
Chan et al. found that certain underlying medical
conditions were associated with subsequent hospitalization after an OU stay.
16
(See Table 29.2.)
Likely organisms in CAP include: Pneumococcus,
Legionella, Mycoplasma, Haemophilus influenzae,
Chlamydia pneumonia, and Moraxella catarrhalis.
16
Antibiotic treatment in the OU continues
the ceftriaxone (1 g IV q 24 h) and a zithromycin
(500 mg IV q 24 h) initiated in the emergency
department. Patients who are penicillin allergic
may be treated with levofloxacin (750 mg
IV q 24 h).
17
If community aspiration pneumonia is suspected treatment should be initiated with
ampicillin/sulbactam (1.5–3gIVq6–8h,
decrease if impaired creatinine clearance) or
clindamycin (600–900 mg q 8 h) for penicillin
allergic patients.
17
Outpatient regimes after the OU stay include:
oral clarithromycin (250–500 q 12 h, decrease if
impaired creatinine clearance), azithromycin (250
mg daily), and as a second-line choice doxycycline
(100 mg q 12 h).
17,18
Respiratory flouroquinolones,
levofloxacin (750 mg daily), may also be used, but
the Centers for Disease Control recommends
reserving these agents for those who cannot tolerate
or have failed other therapy or have significant
comorbidities without criteria for HCAP.
18
Disposition
At the time of discharge patients should be given
a prescription for the appropriate antibiotic as
well as pneumonia home-going instructions. The
patient should be informed as to which symptoms
indicate a worsenin g condition and warrant
a return to the ED. Antipyretics and analgesics
should be prescribed as needed. Follow-up
instructions should be person or clinic specific
and time specific and symptom specific. Instructions regarding modification of routine medications, if any, should also be given.
Summary
Patients presenting to the ED with pneumonia
and placed in the OU should be stable and have
an expected clinical course that will allow discharge within the time constraints of the OU.
Patients that have new hypoxia or hypotension
should not be admitted to the OU. Patients who
are placed on mechanical ventilation should not
be placed in the OU. OU treatment should consist
of antibiotics, analgesics, antipyretics, hydration,
and antiemetics as needed. Treatment of stable
chronic medical conditi ons should also be maintained in the OU. Patients who are improved
and able to go home after treatment may be
discharged with appropriate antibiotics and pneumonia care instructions. Patients who have not
improved sufficiently to go home should be
admitted. There are several pneumonia severity
Table 29.3 Inclusion and Exclusion Criteria for Pneumonia
Patients in an Observation Unit
Inclusion Exclusion
Improved clinical
course in ED
BP < 80 or > 200 systolic
Expected discharge
within time
parameters of the
observation unit
RR > 40
No new symptoms
suspicious for ACS
HR > 140
No pneumothorax Hypoxia (changed from
patient’s baseline if on
home O
2
)
Unit has capabilities to
perform respiratory
assessments
Unable to speak due to
shortness of breath
Unit has capability to
intervene if patient
decompensates
Indecision between ICU
vs. medical floor
Pulse oxygen saturation
< 80 on room air, pH
< 7.3 or > 7.5, pO
2
< 60,
pCO
2
> 50
ECG changes consistent
with ACS
Emergent intubation
Pharmacologic blood
pressure support
Eric Anderson
032
20:58:53
rating scales that will aid the physician in deciding
questionable cases.
The OU admission is useful for the management
of patients who are not quite ill enough to warrant a
full hospital admission but the ED may have reservations about immediate discharge to home. The
OU has been shown to decrease costs of care and
decrease utilization of inpatient beds.
19,20
References
1. Kontou P, Kuti JL, Nicolau DP.
Validation of the infectious
disease society of America/
American Thoracic Society
criteria to predict severe
community-acquired
pneumonia caused by
streptococcus pneumonia.
Am J of Emerg Med 2009;27:
968–974.
2. McCaig LF, Nawar EW.
National Hospital Ambulatory
Medical Care Survey:
2004 emergency department
summary. Adv Data 2006 Jun
23;(372):1–29.
3. Aujesky, D, McCausland JB,
Whittle J, et al. Reasons why
emergency department
providers do not rely on the
pneumonia severity index to
determine the initial site of
treatment for patients with
pneumonia. CID 2009;49:
e100–e108.
4. DeFranco CJ, Cullen KA, Kozak
LJ. National Hospital discharge
survey 2005 annual summary
with detailed diagnosis
and procedure data. Vital
Health Stat 2007; 13(165):
1–209.
5. Chalmers JD, Taylor JK,
Mandal P, et al. Validation of
the infectious diseases society
of America/American thoracic
society minor criteria for
intensive care unit admission
in community acquired
pneumonia patients without
major criteria for
contraindications to intensive
care unit care. CID
2011;53:503–511.
6. Trotter CL, Stuart JM, George
R, et al. Increasing hospital
admissions for pneumonia,
England. Emerg Inf D
2008;14:727–733.
7. Barlett JG, Dowell SF, Mandell
LA, et al. Practice guidelines for
the management of community
acquired pneumonia in
adults. Clin Infect Dis 2000;31:
347–382.
8. Fine MJ, Smith MA, Carson
CA, et al. Prognosis and
outcomes of patients with
community acquired
pneumonia. A meta-analysis.
JAMA 1996;275:134–141.
9. Marrie TJ, WU L. Factors
influencing in hospital mortality
in community acquired
pneumonia: a prospective study
of patients not initially admitted
to the ICU. Chest
2005;127:1260–1270.
10. Infectious Disease Society of
America/American Thoracic
society Consensus, Guidelines
on the management of adults
with community acquired
pneumonia. Am J Respir
Crit Care Med 2001;163:
1730–1754.
11. Nazarian DJ, Eddy OL, Lukens
TW, et al. Clinical Policy:
Critical issues in the
management of adult patients
presenting to the emergency
department with commnity
acquired pneumonia. Ann
Emerg Med 2009;54(5):704–731.
12. Slaven EM, Santanilla JI,
DeBlieux PM. Healthcare
associated pneumonia in the
emergency department. Sem in
Respir and Critical Care Med
2009;(30)1:46–51.
13. Musonda P, Sankaran P,
Subramanian DN, et al.
Prediction of mortality in
community acquired
pneumonia in hospitalized
patients. Am J Med Sciences.
2011;342(6):489–93.
14. Fine MJ, Auble TE, Yealy DM,
et al. A prediction rule to
identify low-risk patients with
community acquired
pneumonia. J Engl J Med.
1997;336:243–250.
15. Myint PK, Bhaniani A,
Bradshaw SM, et al.
Usefulness of shock index and
adjusted shock index in the
severity assessment of
community acquired
pneumonia. Respiration 2009;
77468–77490.
16. Chan, SSW, Yuen, EHY, Kew J,
et al. Community acquired
pneumonia implementationof a
predictionrule to guide selection
of patients for outpatient
treatment. Europe J of Emerg
Med 2001;8: 279–286.
17. Rehm SJ, Sekeres JK, Neuner E,
et al. Cleveland Clinic.
Guidelines for infectious
diseases 2012–2013. Cleveland
Clinic. 2012–2013.
18. Emerman CL, Anderson E,
Cline DM. Community
acquired pneumonia, aspiration
pneumonia and noninfectious
pulmonary infiltrates. In
Emergency Medicine:
AComprehensiveStudyGuide.
Tintinalli J, Stapczynski JS, Ma
J, et al. (eds.). McGraw-Hill
Medical Pub, New York.
2011;7th ed:479–491.
19. Leykum LK, Huerta V,
Mortensen. Implementation of
a hospitalist-run observation
unit and impact on length of
stay (LOS): A brief report. Jof
Hosp Med 2010;5:E2–E5.
20. Rydman RJ, Isola ML, Roberts
R, et al. Emergency department
observation unit versus
hospital inpatient care for a
chronic asthmatic population:
A randomized trial of
health status outcome and
cost. Med Care 1998;36(4):
599–609.
Community Acquired Pneumonia
032
20:58:53
Subpart IVB
Chapter
30
Clinical – Respiratory
Primary Spontaneous Pneumothorax
Chew Yian Chai, MD
Introduction
Spontaneous pneumothoraces have no preceding
traumatic or iatrogeniccause.Theycanbefurther divided into two groups: primary and secondary. Primary spontaneous pneumothoraces
(PSP) occur in people with no underlying parenchymal disease. Some genetic conditions, for
example, Marfan’s Syndrome, predispose
patients to getting pne umothoraces. Secondary
spontaneous pneumothoraces (SSP) tend to
occur in people with underlying parenchymal
disease, for exam ple, COPD.
We discuss the manag ement of PSP in the
observation unit (OU).
Spontaneous pneumothorax occurs from the
rupture of blebs and bullae. It typically occurs in
tall, young people w ithout parenchymal lung disease, and is thought to be related to increased
shear forces in the apex.
Patients typically present with chest pain
and mild shortness of breath. Most patients
are hemodynamically stable, except for those
patients with a hemopneumothorax and/or a
tension pneumothorax, which are medical emergencies that require immediate decompression.
Standard erect chest radiographs (CXR) with
PA and lateral views view in inspiration are
recommended for the in itial diagnosis of pneumothorax, rather than expiratory films (Level A).
2
The size of the pneumothoraces does not correlate well with the clinical manifestations.
2
Therefore the management strategy is determined
by clinical evaluation rather than size of the
pneumothorax.
Small pneumothoraces with minimal symptoms (i.e., not tachypneic or in cardiorespiratory
distress) can be observed as outpatients (Level B),
2
provided they can easily seek medical attention if
there is any deterioration of their symptoms.
Small pneumothoraces are defined as those with
an apex to cupola distance measuring < 3cm
(American guidelines) or interpleural distance at
level of hilum measuring < 2 cm (British guidelines). (See Figure 30.1) Alternatively, they can be
Figure 30.1 Rim of air between lung
and chest wall
(Figure courtesy of Cleveland Clinic Art and
Photo Department)
033
20:58:55
admitted to the OU for supplemental high-flow
oxygen (10 L/min), which can result in a fourfold increase in the rate of pneumothorax resolution, and a repeat CXR next day to assess
interval changes. There is no evidence that active
intervention improves the associated pain,
which can be adequately controlled by appropriate analgesics.
For symptomatic PSP of whatever size, for
example, breathlessness, active intervention –
needle aspiration or chest drain insertion – should
be performed (Level A).
2
According to the American College of Chest
Physicians (ACCP),
1
a pneumothorax is considered large if it measures > 3 cm from the apex
to cupola. Clinical stability is defined as respiratory rate < 24 breaths/min, heart rate > 60/min
or < 120/min, normal blood pressure, room air
oxygen saturation > 90%, and the ability to speak
in full sentences between breaths. Patients with
large PSP, but without significant breathlessness,
may be managed by observation alone – though
most clinicians advocate intervention in order to
speed resolution (Level A).
2
The 2010 British Thoracic Society (BTS)
Guidelines
2
recommends simple needle aspiration
(NA) as the first-line treatment for all symptomatic PSP. NA has shown equivalent success to the
intervention of large-bore chest drains, plus a
reduction in hospital admission and length of stay
(LOS) (Level A).
3,4
Several meta-analyses
5,6,7
were
limited by the small numbers of patients and
studies, and the NA success rates range from
30–80%. NA should cease after aspiration of 2.5
liters of air, as further re-expansion is unlikely due
to ongoing air leak.
2
Repeat CXR is then per-
formed to assess resolution. Failure of resolution
will us ually necessitate a second procedure such as
a small bore chest drain (Level A). Further repeat
NA is unlikely to be successful unless there were
initial technical difficulties, for example, kinked
catheter (Level B).
2
The ease of Seldinger (catheter over guide
wire) chest drains has gained widespread usage
and may be regarded as a simpler option to NA.
Mini chest drains have been shown to have a
similar success rate to larger chest drains,
8–13
but there are no randomized controlled trials
(RCTs) to compare them to NA. In addition, it
is less invasive and greatly improves the patient’s
comfort and cosmetic outcome. Our Center
modifies this technique further, by connecting
the Seldinger chest drain to a three-way adaptor
and underwater seal, hence permitting a “stepwise” approach to the management of PSP. It
allows repeat aspiration via the three-way adaptor
connected to the chest drain, and continuous
drainage to the underwater seal. (Figure 30.2)
(See also Chapter 83 Specialized Clinical Protocols/Guidelines: Spontaneous Pneumothorax)
Figure 30.2 Needle aspiration of
spontaneous pneumothorax
CXR = chest radiograph
COPD = chronic obstructive pulmonary
disease
VATS = video assisted thoracoscopic
surgery
(Figure courtesy of Cleveland Clinic Art and
Photo Department)
Primary Spontaneous Pneumothorax
033
20:58:55
Inclusion Criteria
Patients who are haemodynamically stable, with a
systolic blood pressure > 90 mmHg, and with
SpO2 > 92%
2
will be included.
Exclusion Criteria
Patients with hemodynamic instability, SSP or a
gery (VATS) will be admitted to the inpatient
unit. Pneumothoraces secondary to trauma or
complicated by hemothoraces should also be
admitted to the inpatient unit. If there is a clinical
suspicion of persistent air leak, they should not be
admitted to the OU. Tension pneumothorax and
bilateral pneumothorax are excluded. Pneumothorax with large pleural effusion (hemo/hydropneumothorax) should also be excluded. Patients
with recurrence on the ipsilateral side or contralateral side will benefit from VATS as the recurrence rates have been reported to be as high as
15–40%, and are, therefore, admitted to an inpatient service.
Management/Intervention
Apical Pneumothoraces
For patients with apical pneumothoraces, they
will be administered supplemental oxygen. If the
apex cupola distance is > 2 cm, they will undergo
needle aspiration at the second intercostal space
and have a CXR repeated post aspiration. These
patients will be kept in the OU and have a repeat
CXR at the 14th hour. Following successful resolution, the patient can then be discharged with
early review. (Figure 30.1)
Rim Pneumothoraces
For patients with rim pneumothoraces (presence
of rim of air between lung and chest wall)
(Figure 30.1), a 12F Seldinger chest drain will be
inserted. This is connected to a three-way adaptor
and underwater seal, to allow aspiration(s) and
continuous passive drainage respectively. They
will then be admitted to the OU and placed on
supplemental oxygen. The chest drain will be
clamped at the 12th hour, and a repeat CXR will
be obtained at the 14th hour. For rim pneumothoraces that do not improve after clamping
of the tube, repeat aspiration and underwater
drainage will be continued for a further 6 hours.
The CXR will then be repeated 2 hours post
clamping of the chest tube. (Figure 30.2)
Potential Complications
All patients placed in the OU under a pneumothorax protocol will have their vital signs monitored closely to detect any deterioration or
complications such as hemothorax, tension
pneumothorax (secondary to kinked or blocked
catheter), re-expansion pulmonary edema, or surgical emphysema.
Hemothorax can oc cur due to bleeding from
the bleb after chest drainage, and can be potentially life-threatening if not detected early. This
will warrant immediate surgical referral for VATS
to arrest the bleeding.
Re-expansion pulmonary edema (RPE) can
potentially happen after a rapid expansion of lung
parenchyma following a chest drain insertion for
a especially large PSP that may have been present
for more than a few days.
2
This is thought to be
due to mechanical stress applied to the “injured”
capillaries that are already “leaky.” The patient
typically presents with acute breathlessness and
desaturation, and may cough out frothy sputum.
Clinical examination of patients with RPE may
reveal coarse rales in the affected lung, or less
commonly in the contralateral lung. Management
for RPE is largely supportive with oxygen (consider intubation if indicated) and fluids (NOT
diuresis). The incidence of RPE may be up
to 14% (higher in younger patients with large
PSP). Fatalities have been reported, as high as
20% in one case series report.
19
Thus, one must
be able to recognize RPE, and institute supportive
treatment early.
Surgical emphysema is a well-recognized
complication of chest drains. This is usually selflimiting, and treatment is conservative. It is usually seen with a kinked/blocked chest drain, or in
patients with large air leak on a relatively small
bore chest drain. Very rarely does airway obstruction or thoracic obstruction happen, in which
case one will need to intervene with intubation/
tracheostomy, skin incision decompression or
large-bore chest drain.
Discharge Advice and Follow-Up
Patients with stable apical pneumothoraces will be
discharged the next day. Patients whose pneumothoraces do not show improvement will
Chew Yian Chai
033
20:58:55
subsequently be admitted to the respiratory unit.
For rim pneumothoraces, if the lung shows good
expansion, the chest tube will be removed before
discharge. All patients will be discharged with
pneumothorax advice and followed up by our
respiratory medicine physicians within 2 weeks,
with a CXR on arrival to assess resolution.
Patients who are suspected to have Marfan’s
syndrome will also be referred to the Cardiolog y
Marfan’s clinic for further workup.
All patients discharged after intervention or
otherwise will be given written advice to return
to the Emergency Department if they develop
acute breathlessness or giddiness/syncope. We
also reinforce lifestyle advice on issues such as
smoking, air travel, and diving. Smoking increases
the recurrence risk, and cessation should be
encouraged. Air travel should be avoided until full
resolution (Level C).
2
The BTS guidelines on air
travel emphasize that the recurrence risk only falls
significantly 1 year after the index pneumothorax,
hence, in the absence of definitive surgical procedure, patients may want to defer air travel, as
the consequences of a recurrence during air travel
can be serious. Diving should be permanently
avoided, unless the patient has undergone bilateral
surgical pleurectomy (Level C).
2
Summary
The goal of admitting patients with simple PSP to
the OU is to treat the pneumothorax, monitor
for potential complications and facilitate early
discharge. Both needle aspiration and small
bore chest drains compare favorably with large
bore chest drains. With the use of small bore
Seldinger chest drai ns, chest tube insertion has
become minimally invasive and a much less painful procedure. This has also greatly reduced the
length of stay and improved patient satisfaction.
References
1. Michael H Baumann, Charlie
Strange, John E Heffner,
Richard Light, Thomas J Kirby,
Jeffrey Klein, James D
Luketich, Edward A Panacek,
Steven A Sahn. Management of
spontaneous pneumothorax:
an American College of Chest
Physicians Delphi concensus
statement. Chest 2012,
March 9.
2. Andrew MacDuff, Anthony
Arnold, John Harvey, on behalf
of BTS Pleural Disease
Guideline group. Management
of spontaneous pneumothorax:
British Thoracic Society pleural
disease guideline 2010. BMJ
2012, March 23.
3. Win Sen Kuan, Kanwar Sudhir
Lather, Malcolm Mahadevan.
Primary spontaneous
pneumothorax – the role of
the emergency observation
unit. American Journal of
Emergency Medicine (2011) 29,
293–298.
4. Noppen M, Alexander P,
Driesen P, et al. Manual
aspiration versus chest tube
drainage in first episodes of
primary spontaneous
pneumothorax. Am J Respir
Crit Care Med 2002; 165:
1240–1244.
5. Ayed AK, Chandrasekaran C,
Sukumar M, et al. Aspiration
versus tube drainage in primary
spontaneous pneumothorax: a
randomized study. Eur Resp J
2006; 27:477–482.
6. Devanand A, Koh MS, Ong
TH, et al. Simple aspiration
versus chest-tube insertion in
the management of primary
spontaneous pneumothorax: a
systemic review. Respir Med
2004; 98:579–590.
7. Zehtabchi S, Rios CL.
Management of emergency
department patients with
primary spontaneous
pneumothorax: needle aspiration
or tube thoracostomy? Ann
Emerg Med 2008; 51:91–100.
8. Wakai A, O’ Sullivan RG,
McCabe G. Simple aspiration
versus intercostal tube drainage
for primary spontaneous
pneumothorax in adults.
Cochrane Database of Syst Rev
2007; (1):CD 004479
9. Lai SM, Tee AK. Outpatient
treatment of Primary
Spontaneous Pneumothorax
using a small-bore chest drain
with a Heimlich valve: the
experience of a Singapore
emergency department. Eur
J Emerg Med 2012: 19(6):
400–404.
10. Contou D, Razaki K, Katsahian
S, Maitre B, Meknotso-Dessap
A, Brun-Buisson C, Thille AW.
Small-bore catheter versus
Chest tube drainage for
pneumothorax. Am J Emerg
Med 2012 Jan 2.
11. Fysh ET, Smith NA, Lee YC.
Optimal chest drain size: the
rise of the small-bore pleural
catheter. Semin Respir Crit
Care Med 2010 Dec; 31(6):
760–768.
12. Horsley A, Jones L, White J,
et al. Efficacy and complications
of small-bore, wire-guided
chest drains. Chest 2006; 130
(6):1857–1863.
13. Dernevik L, Roberts D,
Hamraz B, et al. Management
of pneumothorax with a minidrain in ambulatory and
hospitalized patients. Scan
Cardiovasc J 2003; 37:172–176.
14. Vedam H, Barnes DJ.
Comparison of large- and
Primary Spontaneous Pneumothorax
033
20:58:55
small-bore intercostal catheters
in the management of
spontaneous pneumothorax.
Int Med J 2003; 33:
495–499.
15. Baumann, MH. Management
of spontaneous pneumothorax.
Clin Chest Med 2006; 27:
369–381.
16. Valle P, Sullivan M,
Richardson H, Bivins B,
Tomlanovich M. Sequential
treatment of a simple
pnuemothorax. Ann Emerg
Med 1988; 17:
936–947.
17. Matsuura Y, Nomimura T,
Nurikami H, et al. Clinical
evidence of re-expansion
pulmonary oedema. Chest
1991; 100:1562–1566.
18. Pavlin DJ, Nessly MC, Cheney
FW. Increased pulmonary
vascular permeability as a cause
of re-expansion edema in
rabbits. Am Rev Respir Dis
1981; 124:422–427.
19. Mahfood S, Hix WR, Aaron
BL, et al. Re-expansion
pulmonary oedema. Ann
Thorac Surg 1988; 45:
340–345.
20. Maunder RJ, Pierson DJ,
Hudson LD. Subcutaneous and
mediastinal emphysema.
Pathophysiology, diagnosis and
management. Arch Intern Med
1984; 144:1447–1453.
21. Conetta R, Barman AA,
Lakovou C, et al. Acute
ventilator failure from
massive subcutaneous
emphysema. Chest 1993;
104:978–980.
22. British Thoracic Society
Standards of Care Committee.
Managing passengers with
respiratory disease planning
air travel: British Thoracic
Society recommendations.
Thorax 2002; 57:
289–304.
23. British Thoracic Society Fitness
to Dive Group. BTS guidelines
on respiratory aspects of
fitness for diving. Thorax 2003;
58:3–11.
Chew Yian Chai
033
20:58:55
Subpart
IVC
Clinical – Vascular
Editor’s Comments: Venous Thromboembolic Disease:
Deep Vein Thrombosis and Pulmonary Emboli
With the trend toward outpatient care and a concern for cost-effectiveness, the possibility of
using the observation unit for disorders that previously were treated only as an inpatient over
several days has evolved. Patients with pulmonary emboli have generally not been considered
appropriate patients for the observation unit and have previously only been treated on the
hospital inpatient unit. Recently, however, the concept of risk stratification of pulmonary
emboli patients, similar to the risk stratification of chest pain patients, and the management of
low-risk (e.g., hemodynamically stable, non-hypoxic) pulmonary emboli patients in a noninpatient setting, specifically the observation unit, or even as an outpatient, has emerged. Use
of clinical parameters including vital signs with pulse oximetry, and laboratory/ancillary tests
such as troponin, BNP, CT scan, echocardiography or other studies to document normal right
ventricular function and no acute myocardial dysfunction, may allow us to risk stratify these
patients, initiate treatment, and begin patient/family education in the observation unit, thereby
avoiding an inpatient hospital admission.
The next several chapters – 31 Deep Vein Thrombosis, 32 Acute Pulmonary Embolism,
and 33 Anticoagulants – discuss the value of observation medicine for patients with venous
thromboembolic disease, specifically deep vein thrombosis and pulmonary emboli, including
the management of these diseases. There has been a great deal of research recently with these
disorders including the development of newer anticoagulation therapies. These agents are
referred to as NOACs for novel (or newer) oral anticoagulants, or “non-vitamin K antagonist
oral anticoagulants” or DOACs for direct oral anticoagulants or TSOACs for “target specific
oral anticoagulants.” There has also been the introduction of a reversal agent, idarucizumab,
which is a monoclonal antibody antidote specifically for the reversal of the anticoagulant
effects of dabigatran. It is likely that additional agents, both anticoagulants and reversal agents
for other anticoagulants, will be introduced in the near future.
Anticoagulants are agents that inhibit one or more steps in the coagulation cascade. They
have various mechanisms of action. The anticoagulants include unfractionated heparin, low
molecular weight heparins, fondaparinux, vitamin K antagonists, direct thrombin inhibitors,
and direct factor Xa inhibitors; and there are other agents that are in various stages of
development. The oral direct factor Xa inhibitors, which all have an “X” in their name and
all end in “Xa-ban,” include rivaroxaban, apixaban, edoxaban, and betrixaban. The oral direct
thrombin inhibitors (DTIs) include dabigatran.
034
16:03:32
Subpart IVC
Chapter
31
Clinical – Vascular
Deep Vein Thrombosis (DVT)
Carol Lynn Clark, MD MBA FACEP
Michelle A. Wiener, MD MS
Introduction
Pulmonary embolism (PE) and deep vein thrombosis (DVT) are collectively encompassed by
the term venous thromboembolism (VTE), and
occur at an incidence of approximately 0.1% of
persons per year.
1
VTE should be thought of as a
continuum. DVT alone is a major cause of preventable morbidity and mortality worldwide,
accounting for up to 600,000 U.S. hospitalizations
per year.
2
Economically speaking, this translates
into a substantial proportion of health care claims
with an estimated total co st of 2–10 billion dollars
per year in the United States alone, for the period
from 1998 to 2004.
3
The incidence of primary
DVT increases markedly with age, immobility,
and surgery. For cases such as major orthopedic
procedures (joint arthroplasty or hip fracture
surgery) the risk can be as high as 40–60% without prophylaxis.
4
Several other lesser risk factors
have been identified as well, including pregnancy,
obesity, fracture, contraceptives, hematologic
disorders, stroke, and lower extremity trauma.
The most common underlying conditions associated with higher recurrence rates of DVT are
increasing age (> 65 years), body mass index,
cancer, limb paralysis, and an idiopathic first
thrombus.
5, 6
Due to these factors, despite attempts
to decrease the incidence by utilizing evidence
based DVT prophylaxis, the disease burden of
DVT has unfortunately remained constant due to
an aging population, increasing obesity rates, and
improved access to surgical care.
7
Discussion
Early diagnosis and treatment of VTE is essential
in order to reduce the risk of serious complications that are associated with this condition.
While a fatal PE is the most severe and acute
progression of the disease, chronic DVTs may
progress to a potentially debilitating post thrombotic syndrome in as many as 50% of
patients.
8,9,10
In these cases chronic pain, edema,
and skin discoloration/ulceration are a common
result of long-term inflammation and venous
hypertension.
11
These symptoms may be severe
and disabling.
The most common presenting symptoms of
DVT are a combination of lower extremity pain,
tenderness, erythema, and lower calf swelling.
12
However, patients will present to the Emergency
Department (ED) with a wide range of clinical
symptoms, which can make diagnosis difficult.
The presenting symptoms may be as subtle and
nonspecific as calf cramps or swelling. In a study
of 87 patients with negative venograms for suspected DVT, the most common mimicking disorders were identified as muscle strain/tear
(30%), twisting injury to the leg (10%), leg swellinginaparalyzedlimb(9%),lymphangitis/
lymph obstruction (7%), and venous insufficiency (7%).
13
Inseverecasessuchasphlegmasia
cerulea dolens, defined as a massive proximal
thrombotic venous occlusion, symptoms can
include sudden and severe leg pain, swelling,
cyanosis, late stage compartment syndrome, or
systemic circulatory collapse.
Diagnosis often begins with a standardized
clinical model that combines risk factors with
presenting signs and symptoms to subsequently
stratify patients with a suspected DVT into highor low-risk categories. There are many clinical
prediction tools used, but the most commonly
accepted model is the Wells score, which assigns
point values to ten significant clinical variables
in order to create a pre-test probability of
DVT.
14
The p re -test probability will then guide
thechoiceofdiagnosticmodalityincludingDdimer assays, proximal compression ultrasounds
(CUS), whole leg ultrasounds and less frequently
used tests such as, contrast venography, Computer Tomography scan, and Magnetic Resonance Imaging. While choosing a test modality
will depend on cost, availability , and pre-morbid
035
20:59:08
Соседние файлы в папке Библиотека им академика М.И. Перельмана