Dibetes melitus diet

Diet Therapy
1. Diet Therapy in General
 Diet therapy is the cornerstone of therapy for all patients with diabetes. Practicing an appropriate diet
improves glycemic control.1,2 (grade A)
2. Individualized Diet Therapy
 Individualized diet therapy according to the lifestyle of each patient is essential for successful
introduction and continuation of the recommended diet therapy and requires, first and foremost, that
each patient be interviewed adequately about his/her dietary habits, such as food preferences and diet
timetables as well as his/her physical activity level. (grade A; consensus)
○ The elderly are often associated with disturbance of taste, smell, and mastication, reduced secretion of
saliva and gastric acid, and impaired renal and hepatic function, which leads to malnutrition and
sarcopenia. Therefore, it is required that diet therapy for the elderly be so formulated as to avoid the risk
of malnutrition.
3. Diet Instructions by Registered Dietitians
 In clinical practice, diet instructions involving a registered dietitian are useful for glycemic control.3
(grade B)
 The Food Exchange Lists, edited by the Japan Diabetes Society, is commonly used for diet instructions.
However, if it is difficult for patients to understand the Food Exchange Lists, actual food products or food
models may be used to give instructions. (grade B; consensus)
4. Determination of the Amount of Energy Intake
● The amount of energy intake is to be determined by a physician, with consideration given to his/her
glucose levels, blood pressure, serum lipid levels, height, body weight, age, sex, complications, and energy
expenditure (physical activity), as well as the amount of prior food intake. It must be also determined
individually to meet disease conditions of each patient (e.g., setting a lower target for energy intake for
obese or elderly patients). (grade A; consensus)
Equations used for calculation of energy intake:
Amount of energy intake = ideal body weight × physical activity level
Ideal body weight (kg) = [height (m)]2 × 22
Physical activity level (kcal/kg/ideal body weight)
25-30: low-intensity exercise (e.g., jobs involving deskwork)
30-35: moderate-intensity exercise (e.g., jobs involving standing work)
 35: high-intensity exercise (e.g., jobs involving heavy physical work)
5. Composition of Macronutrients
 In formulating a diet for patients with diabetes, it is to be ensured that carbohydrates account for 50-60%
of the total energy4, while proteins account for 1.0 to 1.2 g/kg/ideal body weight, with the rest of the
energy accounted for by fats. (grade A)
○ Carbohydrates: Given that there is a paucity of evidence as to the intake of carbohydrates in Japan and
there is no consensus as to the lower normal limits for carbohydrate intake, it is desirable that
carbohydrates not more than 60% of the total energy intake; that the intake of sweets, jams or soft drinks
be minimized as they contain a large amount of sucrose that leads to an elevation of triglyceride levels;
and that the intake of fruit be limited to up to 1 unit (80kcal)/day, given that fruits currently on markets
often contain a large amount of sugar as a result of selective breeding.
○ Proteins: While there is a paucity of evidence for protein intake, it is common practice to recommend 1.0
to 1.2 g/kg/ideal body weight of proteins. Intake of less animal protein and more plant protein (e.g.,
soybean products) is recommended to prevent atherosclerosis.5 Protein-restricted diet is recommended
for patients with diabetic nephropathy.
 Saturated and polyunsaturated fats: It is recommended that saturated and polyunsaturated fats account
for not more than 7% and 10% of the total energy intake, respectively. (grade B; consensus)
 n-3 polyunsaturated fatty acids (e.g., eicosapentaenoic acid [EPA], docosahexaenoic acid [DHA]) which
abound in fish are shown to be effective in lowering glucose and triglyceride levels.6,7
6. Salt Intake
 Excessive salt intake may lead to the onset of vascular diseases through elevation of blood pressure as
well as to an increase in appetite. Therefore, salt intake should generally be limited, and restricted to 6
g/day in patients with diabetes and hypertension and in those with overt nephropathy or more severe
disease. (grade B; consensus)
7. Dietary Fiber Intake
 Intake of dietary fiber (20 to 25 g/day) is shown to be effective in improving glycemic control as well as in
lowering serum lipid levels (cholesterol and triglycerides).8 (grade B)
 Daily intake of 350 g or more of vegetables should be targeted. During meals, taking vegetables first helps
to reduce postprandial glucose increases, HbA1c values, and body weight.9
8. Intake of Varied Foodstuffs
 To avoid vitamin or mineral deficiency, it is to be ensured that patients take as many kinds of food items
as possible. (grade B; consensus) 

dietary guidelines dm 2 pdf

Praktik diet dm sehari hari pdf

References
1. United Kingdom Prospective Diabetes Study (UKPDS) Group. UK Prospective Diabetes Study 7. Response
of fasting plasma glucose to diet therapy in newly presenting type II diabetic patients. Metabolism
1990;39:905-912. (level 3)
2. Wing RR, Blair EH, Bononi P, et al. Caloric restriction per se is a significant factor in improvements in
glycemic control and insulin sensitivity during weight loss in obese NIDDM patients. Diabetes Care
1994;17:30-36. (level 1)
3. Kulkarni K, Castle G, Gregory R, et al. Nutrition Practice Guidelines for Type 1 Diabetes Mellitus positively
affect dietitian practices and patient outcomes. The Diabetes Care and Education Dietetic Practice Group. J
Am Diet Assoc 1998;98:62-70/quiz 72-74. (level 3)
4. Anderson JW, Randles KM, Kendall CW, et al. Carbohydrate and fiber recommendations for individuals
with diabetes: a quantitative assessment and meta-analysis of the evidence. J Am Coll Nutr 2004;23:5-17.
(level 1)
5. Fung TT, van Dam RM, Hankinson SE et al: Low-carbohydrate diet and all-cause and cause specific
mortality: two cohort studies. Ann Intern Med 153: 289-298, 2010. (level 2)
6. Garg A. High-monounsaturated-fat diets for patients with diabetes mellitus: a meta-analysis. Am J Clin Nutr
1998;67(Suppl):577S-582S. (level 1)
7. Friedberg CE, Janssen MJ, Heine RJ, et al. Fish oil and glycemic control in diabetes: a meta-analysis.
Diabetes Care 1998;21:494-500. (level 1)
8. Chandalia M, Garg A, Lutjohann D et al: Beneficial effects of higher dietary fiber intake in patients with
type 2 diabetes mellitus. N Engl J Med 342:1392-1398, 2000. (level 1)
9. Imai S, Matsuda M, Hasegawa G, et al. A simple meal plan of “eating vegetables before carbohydrates” was
more effective for achieving glycemic control than an exchange-based meal plan in Japanese patients with
type 2 diabetes. Asia Pac J Clin Nutr 2011;20:161-168. (level 3) D I

Diabetes melitus: koas ini raup lebih 0,5 milyar dari korea selatan

Dr priyo begitu panggilannya, setelah beberapa bulan jadi koas rela cuti untuk melakukan penelitian yang di danai dari korea selatan lebih dari 0,5 milyar.
Mahasiswa salah satu universitas ternama di Yogyakarta ini mendapat tawaran mengiyurkan mengenai salah satu tanaman herbal yang tersebar luas di indonesia. Tanaman kelor yang di telitinya menarik perhatian dari kedutaan Korea Selatan yang langsung di persentasikan di Korea. Bersama timnya berangakat ke Korea mempersentasikan proposal penelitian tentang infusan daun kelor. Awalnya pihak korea selatan menawarkan 0,5 milyar, namun disepakati sekitar 700 juta setelah negosiasi. Penelitian ini cukup banyak melibatkan pakar kedokteran mengingat permintaan pihak korea selatan yang menginginkan perluasan manfaat daun kelor untuk gym atau massa otot. Penelitian yang menggunakan peralatan yang rumit inipun terlaksana walau sempat istirahat beberapa minggu untuk menghilangkan kejenuhan yang mengharuskan timnya berlibur ke singapura dan negara sekitarnya. Setelah beberapa bulan penelitian tentang daun kelor inipun dipresentasikan di korea selatan dengan hasil yang memuaskan. Perkembangan obat herbal diabetes melitus dengan daun kelor menjadi alternatif yang praktis bagi penyandang diabetes karena mudahnya tanaman ini ditemukan. Daun kelor mudah dibudidayakan dalam waktu yang singkat. Daun kelor yang ditanam tidak memerlukan perawatan yang kusus dan cukup dikenal mayarakat sehingga mudah dalam sosialisasi manfaat daun kelor. Ini adalah anugrah alam dari Allah SWT atas kemurahannya, semoga kita bisa mensyukurinya.    

Approved: New Antimicrobial Stewardship Standard

The Joint Commission recently announced a new Medication Management (MM)
standard for hospitals, critical access hospitals, and nursing care centers. Stan￾dard MM.09.01.01 addresses antimicrobial stewardship and becomes effective
January 1, 2017.
Current scientific literature emphasizes the need to reduce the use of inap￾propriate antimicrobials in all health care settings due to antimicrobial resistance.
According to the World Health Organization (WHO): “Antimicrobial resistance
threatens the effective prevention and treatment of an ever-increasing range of
infections caused by bacteria, parasites, viruses and fungi.”1
The Centers for Disease
Control and Prevention (CDC) identified that 20%–50% of all antibiotics pre￾scribed in US acute care hospitals are either unnecessary or inappropriate.2
The
CDC has also stated: “Antibiotics are among the most commonly prescribed medi￾cations in nursing homes. Up to 70% of long-term care facilities’ residents receive
an antibiotic every year.”3
On June 2, 2015, The Joint Commission participated in the White House
Forum on Antibiotic Stewardship. The Joint Commission joined representatives
from more than 150 major health care organizations, food companies, retailers, and
animal health organizations at the forum to express commitment for implementing
changes over the next five years to slow the emergence of antibiotic-resistant bacte￾ria, detect resistant strains, preserve the efficacy of existing antibiotics, and prevent
the spread of resistant infections.4
Subsequently, The Joint Commission developed the antimicrobial steward￾ship standard for hospitals, critical access
hospitals, nursing care centers, ambula￾tory care organizations, and office-based
surgery practices and conducted a field
review in November and December
2015. Prior to and during the field
review, Joint Commission staff conducted
stakeholder calls on the proposed antimi￾crobial stewardship standard with several
governmental and professional organiza￾tions, including the Centers for Medicare & Medicaid Services (CMS), the CDC, and the Society for
Healthcare Epidemiology of America (SHEA).
There was significant support for the antimicrobial
stewardship standard for the hospital, critical access hospital,
and nursing care center accreditation programs. Additionally,
CMS is in the process of developing a Condition(s) of Par￾ticipation (CoP) on antimicrobial stewardship for the hospital
and nursing home settings, which therefore aligns the Joint
Commission’s standard with CMS’s plans for a CoP(s) in this
area. In the meantime, the antimicrobial stewardship standard
for Joint Commission–accredited ambulatory care organiza￾tions and office-based surgery practices is still in development.
The approved antimicrobial stewardship standard and
EPs are shown in the box that begins below and will also be
displayed on The Joint Commission website at http://www.
jointcommission.org/standards_information/prepublication_
standards.aspx. In addition, the requirements will be posted
in the fall 2016 E-dition® update and published in the 2017
Comprehensive Accreditation Manual for the Critical Access
Hospital, Hospital, and Nursing Care Center Accreditation
Programs.
Questions regarding the new antimicrobial stewardship
standard may be directed to Kelly Podgorny, DNP, CPHQ, RN,
project director, Department of Standards and Survey Methods,
The Joint Commission, at kpodgorny@jointcommission.org. P
References
1. World Health Organization. Antimicrobial Resistance. (Updated: Apr
2015.) Accessed May 27, 2016. http://www.who.int/mediacentre/
factsheets/fs194/en/#
2. Centers for Disease Control and Prevention. Core Elements of Hospital
Antibiotic Stewardship Programs. Accessed May 27, 2016. http://www.
cdc.gov/getsmart/healthcare/implementation/core-elements.html
3. Centers for Disease Control and Prevention. Antibiotic Use in Nursing
Homes. Nov 5, 2013. Accessed May 27, 2016. http://www.cdc.gov/
getsmart/healthcare/learn-from-others/factsheets/nursing-homes.html
4. The Joint Commission. Joint Commission Joins White House Effort to
Reduce Antibiotic Overuse. Jt Comm Perspect. 2015 Jul;35(7):4, 11.

Standard MM.09.01.01
The [critical access] hospital has an antimicrobial stewardship
program based on current scientific literature.
Elements of Performance for MM.09.01.01
1. Leaders establish antimicrobial stewardship as an orga￾nizational priority. (See also LD.01.03.01, EP 5)
Note: Examples of leadership commitment to an antimi￾crobial stewardship program are as follows:
l Accountability documents
l Budget plans
l Infection prevention plans
l Performance improvement plans
l Strategic plans
l Using the electronic health record to collect antimi￾crobial stewardship data
2. The [critical access] hospital educates staff and li￾censed independent practitioners involved in antimicro￾bial ordering, dispensing, administration, and monitor￾ing about antimicrobial resistance and antimicrobial
stewardship practices. Education occurs upon hire or
granting of initial privileges and periodically thereafter,
based on organizational need.
3. The [critical access] hospital educates patients, and
their families as needed, regarding the appropriate use
of antimicrobial medications, including antibiotics. (For
more information on patient education, refer to Stan dard PC.02.03.01)
Note: An example of an educational tool that can be
used for patients and families includes the Centers for
Disease Control and Prevention’s Get Smart docu￾ment, “Viruses or Bacteria—What’s got you sick? at
http://www.cdc.gov/getsmart/community/downloads/
getsmart-chart.pdf.
4. The [critical access] hospital has an antimicrobial stew￾ardship multidisciplinary team that includes the follow￾ing members, when available in the setting:
l Infectious disease physician
l Infection preventionist(s)
l Pharmacist(s)
l Practitioner
Note 1: Part-time or consultant staff are acceptable as
members of the antimicrobial stewardship multidisci￾plinary team.
Note 2: Telehealth staff are acceptable as members of
the antimicrobial stewardship multidisciplinary team.
5. D The [critical access] hospital’s antimicrobial steward￾ship program includes the following core elements:
l Leadership commitment: Dedicating necessary hu￾man, financial, and information technology resources.
l Accountability: Appointing a single leader respon￾sible for program outcomes. Experience with suc￾cessful programs shows that a physician leader is
effective.
l Drug expertise: Appointing a single pharmacist leader
responsible for working to improve antibiotic use.
l Action: Implementing recommended actions, such
as systemic evaluation of ongoing treatment need,
after a set period of initial treatment (for example,
“antibiotic time out” after 48 hours).
l Tracking: Monitoring the antimicrobial stewardship
program, which may include information on antibi￾otic prescribing and resistance patterns.
l Reporting: Regularly reporting information on the
antimicrobial stewardship program, which may
include information on antibiotic use and resistance,
to doctors, nurses, and relevant staff.
l Education: Educating practitioners, staff, and
patients on the antimicrobial program, which may
include information about resistance and optimal
prescribing. (See also IC.02.01.01, EP 1 and
NPSG.07.03.01, EP 5)
Note: These core elements were cited from the Centers
for Disease Control and Prevention’s Core Elements of
Hospital Antibiotic Stewardship Programs (http://www.
cdc.gov/getsmart/healthcare/pdfs/core-elements.pdf).
The Joint Commission recommends that organizations
use this document when designing their antimicrobial
stewardship program.
6. D The [critical access] hospital’s antimicrobial steward￾ship program uses organization-approved multidisci￾plinary protocols (for example, policies and procedures).
Note: Examples of protocols are as follows:
l Antibiotic Formulary Restrictions
l Assessment of Appropriateness of Antibiotics for
Community-Acquired Pneumonia
l Assessment of Appropriateness of Antibiotics for
Skin and Soft Tissue Infections
l Assessment of Appropriateness of Antibiotics for
Urinary Tract Infections
l Care of the Patient with Clostridium difficile (c.-diff)
l Guidelines for Antimicrobial Use in Adults
l Guidelines for Antimicrobial Use in Pediatrics
l Plan for Parenteral to Oral Antibiotic Conversion
l Preauthorization Requirements for Specific
Antimicrobials
l Use of Prophylactic Antibiotics
7. D The [critical access] hospital collects, analyzes, and
reports data on its antimicrobial stewardship program.
Note: Examples of topics to collect and analyze data
on may include evaluation of the antimicrobial steward￾ship program, antimicrobial prescribing patterns, and
antimicrobial resistance patterns.
8. D The [critical access] hospital takes action on im￾provement opportunities identified in its antimicrobial
stewardship program. (See also MM.08.01.01, EP 6)

Applicable to Nursing Care Centers
Effective January 1, 2017
Medication Management (MM)
Standard MM.09.01.01
The organization has an antimicrobial stewardship program
based on current scientific literature.
Elements of Performance for MM.09.01.01
1. Leaders establish antimicrobial stewardship as an orga￾nizational priority. (See also LD.01.03.01, EP 5)
Note: Examples of leadership commitment to an antimi￾crobial stewardship program are as follows:
l Accountability documents
l Budget plans
l Infection prevention plans
l Performance improvement plans
l Strategic plans
l Using the electronic health record to collect antimi￾crobial stewardship data
2. The organization educates staff and licensed inde￾pendent practitioners involved in antimicrobial order￾ing, dispensing, administration, and monitoring about
antimicrobial resistance and antimicrobial stewardship
practices. Education occurs upon hire or granting of
initial privileges and periodically thereafter, based on
organizational need.
3. The organization educates residents, and their families
as needed, regarding the appropriate use of antimi￾crobial medications, including antibiotics. (For more
information on patient and resident education, refer to
Standard PC.02.03.01)
Note: An example of an educational tool that can be
used for patients and families includes the Centers for
Disease Control and Prevention’s Get Smart docu￾ment, “Viruses or Bacteria—What’s got you sick? at
http://www.cdc.gov/getsmart/community/downloads/
getsmart-chart.pdf.
4. The organization has an antimicrobial stewardship mul￾tidisciplinary team that includes the following members,
when available in the setting:
l Infectious disease physician
l Infection preventionist(s)
l Pharmacist(s)
l Practitioner
Note 1: Part-time or consultant staff are acceptable as
members of the antimicrobial stewardship multidisci￾plinary team.
Note 2: Telehealth staff are acceptable as members of
the antimicrobial stewardship multidisciplinary team.
5. D The organization’s antimicrobial stewardship pro￾gram includes the following core elements:
l Leadership commitment: Demonstrate support and
commitment to safe and appropriate antibiotic use
in your facility.
l Accountability: Identify physician, nursing, and phar￾macy leads responsible for promoting and oversee￾ing antibiotic stewardship activities in your facility.
l Drug expertise: Establish access to consultant
pharmacists or other individuals with experience or
training in antibiotic stewardship for your facility.
l Action: Implement policy or practice changes to
improve antibiotic use.
l Tracking: Monitor and measure the use of antibiotic
use and at least one outcome from antibiotic use in
your facility.
l Reporting: Regularly reporting information on the
antimicrobial stewardship program, which may
include antibiotic use and resistance, to physicians
and other practitioners, nurses, and relevant staff.
l Education: Provide resources to physicians and
other practitioners, nursing staff, residents, and
families about antibiotic resistance and opportunities
for improving antibiotic use. (See also IC.02.01.01,
EP 1)
Note: These core elements were cited from the Centers
for Disease Control and Prevention’s The Core Ele￾ments of Antibiotic Stewardship for Nursing Homes
(http://www.cdc.gov/longtermcare/prevention/antibiotic￾stewardship.html). The Joint Commission recommends
that nursing care centers use this document when
designing their antimicrobial stewardship program.
6. D The organization’s antimicrobial stewardship pro￾gram uses organization-approved multidisciplinary
protocols (for example, policies and procedures).
Note: Examples of protocols are as follows:
l Antibiotic Formulary Restrictions
l Assessment of Appropriateness of Antibiotics for
Community-Acquired Pneumonia
l Assessment of Appropriateness of Antibiotics for
Skin and Soft Tissue Infections
l Care of the Long Term Care Patient with a Urinary
Tract Infection
l Care of the Patient with Clostridium difficile (c.-diff)
l Facility Guidelines for Antimicrobial Use in Adults
l Plan for Parenteral to Oral Antibiotic Conversion
l Preauthorization Requirements for Specific
Antimicrobials
7. D The organization collects, analyzes, and reports data
on its antimicrobial stewardship program.
Note: Examples of topics to collect and analyze data
on may include evaluation of the antimicrobial steward￾ship program, antimicrobial prescribing patterns, and
antimicrobial resistance patterns.
8. D The organization takes action on improvement op￾portunities identified in its antimicrobial stewardship
program. (See also MM.08.01.01, EP 6)

Ex vivo culture of human atherosclerotic plaques: A model to study immune cells in atherogenesis

Ex vivo culture of human atherosclerotic plaques: A model to study immune
cells in atherogenesis

Abstract
Background and aims: The mechanisms that drive atherosclerotic plaque progression
and destabilization in humans remain largely unknown. Laboratory models are
needed to study these mechanisms under controlled conditions. The aim of this study
was to establish a new ex vivo model of human atherosclerotic plaques that
preserves the main cell types in plaques and the extracellular components in the
context of native cytoarchitecture.
Methods: Atherosclerotic plaques from carotid arteries of 28 patients undergoing
carotid endarterectomy were dissected and cultured. At various time-points, samples
were collected and analysed histologically. After enzymatic digestion, single cells
were analysed with flow cytometry. Moreover, tissue cytokine production was
evaluated.
Results: We optimised the plaque dissection protocol by cutting plaques into circular
segments that we cultured on collagen rafts at the medium–air interface, thus
keeping them well oxygenated. With this technique, the relative presence of T and B
lymphocytes did not change significantly during culture, and the sizes of lymphocyte
subsets remained stable after day 4 of culture. Macrophages, smooth muscle cells,
and fibroblasts with collagen fibres, as well as both T and B lymphocyte subsets and
CD16 natural killer cells, remained largely preserved for 19 days of culture, with a
continuous production of inflammatory cytokines and chemokines.
Conclusions: Our new model of ex vivo human atherosclerotic plaques, which
preserves the main subsets of immune cells in the context of tissue cytoarchitecture,
may be used to investigate important aspects of atherogenesis, in particular, the
functions of immune cells under controlled laboratory conditions.

Introduction
Atherosclerosis and its cardiac and cerebral complications are the leading
causes of death from cardiovascular diseases. For a long time, accumulation of
modified lipoproteins within the arterial wall was considered to be the main cause of
atherosclerotic disease [1]. More recently, however, cells of various types, such as
smooth muscle cells, macrophages, and T cells, have been found to play an
important role in atherosclerotic plaque formation [2]. Moreover, a currently accepted
theory of atherogenesis emphasizes the role of immune system activation caused by
oxidized lipoproteins, which activate endothelial cells (as do other foreign agents
within the vascular wall) [3,4]. It is thought that immune cells are attracted by
chemokines, which are produced by activated endothelial cells, and migrate into the
subendothelium, where they proliferate, leading to atherosclerotic plaque progression
[2,5–7].
The role of immune cells in the growth of plaques has been confirmed in
experimental models on immunodeficient mice, as well as from the presence of
autologous antibodies against oxidized low density lipoproteins in atherosclerotic
plaques [8,9]. In our earlier work, we demonstrated T lymphocyte activation in human
atherosclerotic plaques in comparison with the blood of the same patients [10], thus
providing further evidence for the involvement of the immune system in
atherogenesis.
Despite plentiful evidence for the critical role of the immune system in
atherosclerosis, many important aspects of this phenomenon remain unknown. The
lack of this knowledge is in part due to limitations on access to human atherosclerotic
plaques in vivo, while animal models are often not adequate because of differences

in structures of arterial walls [11,12]. In vitro laboratory-controlled systems are
required for the study of atherosclerotic plaque formation and rupture. Several such
models with cells of only one or two types cultured together have been suggested
[13,14]; however, none of them faithfully reproduces the whole range of intercellular
interactions within human atherosclerotic plaques [15,16].
Here, we describe a new ex vivo model of human atherosclerotic plaques,
which preserves the main cell types of plaques in vivo, together with the general
tissue cytoarchitecture. We think that this model may prove useful for investigation of
immune cell function in atherogenesis and for development of novel therapeutic
approaches to atherosclerosis treatment.
Materials and methods
For a detailed description of the Materials and methods see Supplementary Data.
Patients
We collected atherosclerotic plaques from carotid arteries of 28 patients with
peripheral artery disease, undergoing carotid endarterectomy because of extended
atherosclerosis (19 men and 9 women; mean age ± standard deviation = 65.4 ± 8.5
years). The degree of carotid artery stenosis varied from 65% to 90% (median
90.0%, interquartile range (IQR) 73.8% to 90.0%). Ten patients suffered from
transient ischemic attack or stroke within 5 years before surgery, and more than half
of all plaque specimens (60.7%) were ruptured, as determined from macroscopic
evaluation. All patients’ characteristics are presented in Supplementary Table1.
This protocol was approved by the A.I. Yevdokimov Moscow State University
of Medicine and Dentistry Ethics Committee. All the participants provided written
informed consent.

Tissue processing
Our work was based on the pioneer work of Dr. Hoffman [17,18], who
developed the technique of histoculture that makes possible maintenance of blocks
of mammalian tissues for weeks at the air–liquid interface.
According to the protocol, surgical atherosclerotic plaque samples were
dissected and divided into three parts: one part of the material was fixed in 4%
formaldehyde (Pierce, Thermo Fisher Scientific, Waltham, MA, USA, cat. 28908) and
embedded in paraffin for histological examination, the second part was digested with
an enzymatic cocktail into a single-cell suspension for flow cytometry. The third part
was dissected, placed on a wetted collagen sponge raft (Pfizer, New York, NY, USA,
cat. 0315-08) at the medium–air interface, and cultured. After one day of culture, and
then every 3rd day, culture medium was collected and replaced with fresh medium.
Every 3rd day, several tissue blocks were analysed histologically and by means of
flow cytometry.

Histology
Histology, histochemistry, and immunohistochemistry were performed
according to standard techniques. We focused on several cell types that could not be
properly isolated from plaques by enzymatic treatment and thus were not analysed
with flow cytometry. In particular, we assessed fibroblasts and collagen tissue,
macrophages, and smooth muscle cells, using Masson’s Trichrome staining (Agilent
Technologies, Santa Clara, CA, USA, cat. AR17392-2), antibodies against CD68
(clone KP1, Agilent Technologies) and α-smooth muscle actin (α-SMA) (clone 1A4,
Agilent Technologies), respectively


Statistical analyses

The data obtained in the present study were not normally distributed, according
to the Shapiro-Wilk test, and are presented as medians and IQR. Since distributions
were not normal, for comparison of two independent groups we used the Mann￾Whitney rank test, and for dependent groups we used the Wilcoxon matched pair
test, Friedman ANOVA, and Kendall test. To assess between-group effects, we used
a multiple comparisons rank test. For the age distribution, we made the assumption
of its normality. Statistical analysis was performed with Statistica 10.0 (Statsoft,
Tulsa, OK, USA) and SPSS Statistics 21.0 (IBM, Armonk, NY, USA). Values of p
<0.05 were considered statistically significant.


Results
Histology of ex vivo plaques
Initially, we separated atherosclerotic plaques from normal artery tissue and
dissected them into ~2-mm cubic blocks for culture, similarly to what was
successfully used earlier to culture various human tissues ex vivo [17,19]. However,
analysis of stained histological sections showed that the viability of cultured tissue

blocks of this size decreased over 8–12 days, and cultured blocks contained only ~20
live cells per 100 mg of tissue (Supplementary Fig.3).
We thought that the tissues might be damaged during dissection into small
blocks. Therefore, to diminish tissue injury during preparation, we modified our
protocol and instead of dissecting into small blocks, we sliced tissue into ring-shaped
2-mm thick segments, and with a diameter depending of the carotid artery size (Fig.
1). To verify tissue viability, every 3rd day several dissected segments were analysed
histologically and by means of flow cytometry.
Analysis of histological sections showed that the dissection of plaques into
large circular segments significantly increased cell survival: tissues were preserved
for 19 days. For histological evaluation, tissue segments were stained with
hematoxylin and eosin, Masson’s Trichrome, anti-CD68, and anti-α-SMA antibodies
and their morphology was assessed as described in Materials and methods. We
found that these plaque segments retained their gross morphology and appeared
viable for more than 19 days of culture. In particular, the integrity of the endothelium
and internal elastic membrane, which are most sensitive to the culture conditions,
were preserved over 19 days of culture without a significant increase in the necrotic
core area (Fig. 2).
Furthermore, in 6 plaques, we quantified areas reacting with aniline blue, anti￾CD68, and anti-α-SMA at days 0, 4, 7, and 19 (Fig. 3). We identified macrophages,
fibroblasts, and smooth muscle cells, along with the endothelium, until day 19 of
culture. We found no statistically significant changes (p >0.05) in the fraction of these
cells during the entire culture period (Table 1).

In plaque samples from 16 donors, we assessed tissue viability using flow
cytometry by analysing immune cells extracted from plaque tissue. We compared
flow cytometry results at day 0 with those at days 4, 7, and 19. Towards this goal, we
digested plaque segments with an enzymatic cocktail containing collagenase XI and
desoxyribonuclease I, washed isolated cells, and stained them with live/dead staining
and monoclonal antibodies against CD45, CD3, CD19, CD4, CD8, and CD16. Two
plaques were excluded from the analysis because of a low cellularity at day 0 (lower
than 500 live cells per 100 mg of tissue).
Analysis of tissue at day 0 revealed a median of 6,286.0, IQR [3,172.1–
12,918.9] lymphocytes per 100 mg of plaque tissue. The absolute numbers and
percentages of B lymphocytes among all lymphocytes at day 0 were significantly
lower than those of T lymphocytes (24.6 [7.8–55.3] cells/100 mg vs. 5,694.1
[2,226.7–11,726.6] cells/100 mg; 0.4% [0.1%–0.5%] vs. 89.6% [84.3%–91.2%],
p=0.001). At day 0, among T lymphocytes, the fraction of CD4+CD8- cells was larger
than the fraction of CD4-CD8+ cells (51.6% [43.8%–58.9%] vs. 39.9% [30.0%–
45.1%], p=0.041). The median amount of CD16 NK cells at day 0 was 58.6 [18.7–
360.9] per 100 mg of plaque tissue (Fig. 4). Consecutive flow cytometry after day 0
was performed in plaques from 8 patients, four of which were cultured until day 19.
We showed that,after a decrease during the first 4 days of culture (n=8, 4,125.8
[2,771.4–6,286.0] cells/100 mg at day 0 vs. 2,619.3 [1,360.8–3,712.2] cells/100 mg
at day 4, p=0.036), the amounts of lymphocytes stabilized and did not change
significantly until the 7th day of culture (n=8, 1,249.6 [445.5–3,706.0] cells/100 mg;
p=0.161). A similar pattern was found in T cells, with a stabilization of their amounts
after a reduction during the first 4 days of culture (n=8, 3,546.5 [2,194.2–5,694.1]
cells/100 mg at day 0 vs. 2,123.4 [1,210.5–3,280.1] cells/100 mg at day 4, p=0.036
vs. 949.5 [375.1–2,378.3] cells/100 mg at day 7, p=0.124). In addition, we found no

significant changes in the amounts of B cells during the first days of culture (n=8,
12.2 [5.3–35.3] cells/100 mg at day 0 vs. 5.6 [3.3–37.2] cells/100 mg at day 4 vs.
7.9 [0.0–11.4] cells/100 mg at day 7, p=0.798). Furthermore, both T and B cells were
also preserved in plaque tissues during 19 days of culture, although their ratio
changed slightly because of the decrease in the number of T lymphocytes (n=4,
7,673.4 [3,789.0–14,813.2] cells/100 mg vs. 2,594.5 [1,926.8–7,569.0] cells/100 mg
for T cells, and 25.8 [5.3–57.9] cells/100 mg vs. 31.0 [12.2–91.2] cells/100 mg for B
cells). CD16 NK cells were found at day 19 as well: the median cell count at the last
day of culture constituted 44.9 [21.9–233.0] cells/100 mg (Fig. 5). We presume that
the initial fall in T cell count may originate from the intense effect of tissue dissection,
while the statistically significant decrease in the amounts of B cells and CD16 NK
cells may not have been revealed because of the small size of these cell subsets.
These changes were followed by a subsequent system stabilization. This was also
evident by the lack of significant changes (p=0.417) in the fraction of dead cells,
which even at day 19 remained at the level of on average 11.2% [10.1%–14.6%].
Importantly, the initial drop in T cell count was not accompanied by significant
changes in the fraction of T cells among all lymphocytes (n=8, 89.6% [76.3%–91.2%]
at day 0 vs. 86.2% [81.1%–90.8%] at day 4, p=0.779; vs. 86.0% [77.5%–86.9%] at
day 7, p=0.674) (Fig. 6A). The decrease in T cell numbers during the first days of
culture was predominantly associated with the reduction of the fraction of CD4 T cells
(n=7, 58.0% [43.8%–63.6%] at day 0 vs. 42.0% [31.4%–49.2%] at day 4, p=0.018;
vs. 40.8% [21.6%–48.7%] at day 7, p=0.018), accompanied by a minor rise in the
fraction of CD8 T cells (n=7, 36.0% [30.0%–47.5%] at day 0 vs. 45.2% [35.3%–
48.6%] at day 4, p=0.063; vs 44.4% [37.9%–55.1%] at day 7, p=0.018) (Figure 6B).
As a result of these changes, the CD4+CD8-/CD4-CD8+ ratio decreased slightly
during culture. As of the 19th day of culture, the fraction of CD4 T cells was reduced

with a concurrent increase in the fraction of CD8 T cells (49.7% [40.2%–57.6%] vs.
42.3% [27.8%–51.9%] for CD4 T cells, and 43.6% [36.1%–53.8%] vs. 50.8%
[40.9%–61.9%] for CD8 T cells) (Figure 7). Nevertheless, both CD4 and CD8 T cells
were also preserved in culture for at least 19 days.
Cytokine production by plaques ex vivo
We analysed the concentrations of cytokines and chemokines released by six
cultured plaques and accumulated in the culture medium from day 1 to day 4 and
from day 16 to day 19 when the medium was changed. We found that in our system
plaques produce substantial amounts of interleukin (IL)-1α, IL-6, IL-8, IL-16, IL-18, IL-
21, IL-22, eotaxin, interferon-λ, granulocyte macrophage colony-stimulating factor
(GM-CSF), macrophage-CSF, tumor necrosis factor (TNF)-α, transforming growth
factor (TGF)-β, growth related oncogene (GRO)-α, interferon gamma-inducible
protein-10, monocyte chemoattractant protein-1, monokine induced by gamma
interferon, macrophage inflammatory protein (MIP)-1α, MIP-1β, and RANTES. In
contrast, the concentrations of the other measured cytokines and chemokines were
lower than the detection limit of the Luminex platform for these analytes.
Within the panel of cytokines and chemokines that were detectable in the
culture medium, we found no significant changes during culture in most of the
cytokines, except for IL-16 and several cytokines whose concentration decreased, in
particular IL-8 (n=6, from 25,698.7 [14,817.3–52,553.3] pg/ml on day 4 to 4,273.1
[2,695.6–6,274.2] pg/ml on day 19), and to a lesser extent GM-CSF, TNF-α, and
GRO-α. At the same time, the concentrations of other cytokines (including eotaxin,
TGF-β, and MIP-1β) increased during culture (Supplementary Table 2).


DI 

Sinau

http://pionas.pom.go.id/info-bpom

Basic mechanical ventilation

Basic Mechanical Ventilation
Jairo I. Santanilla, MD Clinical Assistant Professor of Medicine Section of Emergency Medicine Section of Pulmonary/Critical Care Medicine LSUHSC New Orleans & Section of Critical Care Medicine Ochsner Medical Center

Outline
Outline
Basic Science
Lingo
Initial Settings
Common Intern Mistakes

How do we breath?
Brainstem control
Chemoreceptors
Diaphragm contraction and Chest wall expansion  increased intrathoracic volume
Leads to negative intrathoracic pressure
Air flows from high to low pressure
Negative pressure ventilation

Why do we breath?
Duh
Oxygenation
Ventilation – the exchange of CO2

Important Principles
Ventilation/Perfusion Matching
Ventilation without Perfusion
Dead space ventilation
Perfusion without ventilation
Shunt
Ideal Body Weight (kg)
Males: IBW = 50 kg + 2.3 kg for each inch over 5 feet.
Females: IBW = 45.5 kg + 2.3 kg for each inch over 5 feet.

Why do people need ventilators?
Loss of airway anatomy
Edema, direct/indirect trauma, burns, infection
Loss of protective airway mechanisms
Intoxicants, brain injury, strokes
Inability to oxygenate appropriately
Shunt, alveoli filled with stuff
Inability to ventilate appropriately
Expected clinical course

Basic Ventilator Lingo
Control breath
Vent initiates the breath
Assist breath
the patient initiates the breath

What can I set?
Ventilator Target
Ventilator Mode
Respiratory Rate
PEEP
FiO2
Flow Rate
Other stuff… more later

Step 1: What is the target?
You pick what the ventilator is trying to attain
If the vent is trying to reach a Volume goal, its called Volume-Targeted
AKA volume-cycled, volume-assist, volume- control, volume-limited.
If the vent is trying to reach a Pressure goal, its called Pressure-Targeted
AKA pressure-cycled, pressure-assist, pressure- control, pressure-limited
Most adult ICUs use Volume-Targeted and most PICUs use Pressure-Targeted

Associations of the Emergency Severity Index triage categories with patients’ vital signs at triage: a prospective observational study

Associations of the Emergency Severity Index triage categories with patients’ vital signs at triage:
a prospective observational study

Ineke van der Wulp, Hebe A A Rullmann, Luke P H Leenen, Henk F van Stel

ABSTRACT
Study objective Previous studies on the construct validity of the Emergency Severity Index (ESI) were focused on outcome measures which could not be obtained directly at triage. A study was conducted to the construct validity of the ESI by measuring the association between the ESI triage categories and patients’ vital signs at triage.
Methods A prospective observational study was conducted at an emergency department (ED) in the Netherlands. All patients who entered the ED between 20 July 2009 and 21 August 2009 were eligible for inclusion in the study. Patients’ vital signs, triage category, age, gender, referrer and main complaint were registered. Vital signs were scored according to the Worthing Physiological Scoring System (WPSS) and the numerical pain rating scale. The data were analysed using ordinal logistic regression analyses.
Results An association was found between ESI triage categories and patients’ vital signs at triage. Patients in WPSS categories ‘urgent’ and ‘alert’ were more likely triaged into the urgent triage categories (ESI triage categories 1 and 2) than patients with normal WPSS scores. However, no associations were found between pain scores and ESI triage categories.
Conclusion This study supports the validity of the ESI as it showed that patients’ vital signs are associated with the ESI triage categories. However, a revision of the ESI guidelines concerning pain assessments is necessary.
INTRODUCTION
To sort the increasing number of patients presenting to emergency departments (EDs) on the urgency of their complaints, several triage systems have been developed and implemented.1e8 Frequently mentioned triage systems in the literature are: the Australasian Triage Scale, the Manchester Triage System, the Canadian Triage and Acuity Scale and the Emergency Severity Index (ESI).7910 Compared to other triage systems, the ESI is different in that, as well as the level of urgency, it estimates the number of resources that patients need. ESI resources are defined as laboratory tests, radiology, intravenous fluids, specialty consultation, a simple or complex procedure and intravenous, intramuscular or nebulised medications. Patients can be allocated into five urgency categories. ESI categories 1 and 2 represent patients who need immediate life saving interventions (eg, defibrillation), or patients at an increased risk for deterioration (eg, patients with severe pain). When ESI
categories 1 or 2 criteria are not met, the triage nurse estimates the number of ESI resources that patients need. In case more than one resource is needed, or when vital signs are in a predefined danger zone, patients are triaged into ESI category 3. Moreover, the triage nurse can decide to triage a patient in ESI category 2 on the basis of disturbed vital signs, even though initially the criteria for ESI category 2 were not met. Patients are triaged in ESI categories 4 and 5 when one or no resources are required respectively.11
For reasons of patient safety, it is important that ED triage systems are reliable and valid. Previous studies of the reliability of the ESI reported
k scores12 representing moderate to almost perfect reliability.3481013e16 The reliability places an upper limit on the validity of triage systems, that is, a triage system which produces different urgency scores when used in the same patient cannot be valid.17 The validity of the ESI has mainly been studied by means of construct validity because a gold standard to measure criterion validity is absent. The construct validity has been studied by measuring associations between the ESI triage categories and factors related to urgency. Previous studies have reported such associations of the ESI with actual ED resource usage, ED and hospital length of stay, hospital admission, mortality, survival after an ED visit and physiological measurements.124e81014e16 18 19 However, a limitation of these studies is the focus on outcomes of care because of the time lag between the moment of triage and the reported outcomes. As a result, other factors could have influenced the associations since the patient’s condition could have been changed between arrival in, and departure from the ED. To reduce this bias in triage validity studies, one could focus on measures that can be obtained directly at triage. Furthermore, because of the focus on construct validity in the validation of ED triage systems, it is important to keep studying different constructs, as construct validity is a process of making and testing inferences.17 Although vital signs play an important role in the ESI, no studies have assessed if vital signs are associated with urgency categories. Therefore, a study was conducted to the construct validity of the ESI by measuring the associations between the ESI triage categories and patients’ vital signs at triage. We hypothesised that patients triaged in the urgent triage categories of the ESI were more likely to have disturbed vital signs, and therefore at increased risk for dying in the ED, than patients triaged in less urgent triage categories.
METHODS
Study design
The study was conducted in a prospective observational design. The protocol was reviewed and approved by the medical ethics committee of the University Medical Center Utrecht. Informed consent was obtained from patients before inclusion in the study.
Study setting and population
The study was conducted at the ED of the University Medical Center Utrecht, which is a designated level one trauma centre in the Netherlands. Severely injured patients in the designated trauma region are transported to this ED. The ED is staffed 24 h a day by six full time attending physicians and has an annual census of 21000 patients. The ESI was implemented in 2008 and nurses received a 1-day training course on how to triage with the ESI before implementation. All patients over 16 years of age who entered the ED of the University Medical Center Utrecht on weekdays between 20 July 2009 and 21 August 2009 were included in the study.
Data collection
The data were prospectively collected by one researcher (HR) from Monday to Friday, 09:00 to 17:00 (4 days a week) and from 12:00 to 20:00 (1 day a week). A sample size calculation for regression analysis20 estimated a minimum required sample size of 445 patients. A drop out rate of 10% due to unforeseen circumstances was taken into account in this calculation. Each patient was triaged by the triage nurse on duty and assigned a triage category using standard procedures. Immediately after the triage nurse finished the triage assessment and reported the ESI triage category, the researcher registered patients’ gender, referrer, main complaint, age and measured vital signs that were not measured by the triage nurse. The following vital signs were registered: blood pressure, pulse rate, respiratory rate, oxygen saturation, temperature, the Alert, Voice, Pain and Unconsciousness score, and pain. They were measured using an automated vital signs monitor, a tympanic thermometer and the numerical pain rating scale. The numerical pain rating scale was scored by asking patients to allocate a score between 0 and 10, with 0 indicating no pain and 10 the worst pain imaginable. The researcher was trained in the use of these instruments by a triage nurse during a 1 day training in the ED prior to data collection. In case a patient needed to be seen by a doctor immediately, the patient’s data were collected by the triage nurse. All the data were registered on a form.
Interpretation of vital signs
The ESI guidelines state that the interpretation of vital signs for allocating a patient to ESI categories 2 or 3 is up to the triage nurse, for example, a patient with disturbed vital signs does not automatically meet ESI level 2 criteria.11 For example, a patient who has a history of COPD and presents with an oxygen saturation of 89% might not meet ESI level 2 criteria. However, another patient with the same complaints but no such history does require ESI level 2 criteria when presenting with such an oxygen saturation level. Interpreting vital signs separately is not useful in this study as disturbed vital signs are not necessarily related to higher urgency or life threatening situations. Therefore, a prognostic scoring system in which vital signs were interpreted in relation to short term mortality was applied in this study. The Worthing Physiological Scoring System (WPSS) is such a prognostic scoring system (table 1). The WPSS is based upon identifying physiological markers for mortality at an early stage to undertake timely action. The system has been derived

from and prospectively validated in ED patients and is therefore suitable for use in this study.21 Except for pain, the system consists of the vital signs used in the ESI as well as systolic blood pressure.
Data analysis
The data were analysed by means of ordinal logistic regression analyses.22 Ordinal logistic regression analysis is an extension of binary logistic regression analysis and used in case the dependent variable is ordinal. The effects of the independent variables are interpreted by assuming that they are constant over the categories of the dependent variable, that is the assumption of parallel lines. This is an important assumption and was checked in the analysis. Because of this assumption the analyses were performed using the complementary log-log link function. This link function is used when the higher categories of the dependent variable (eg, the lower urgency categories) are more common. As a result, the associations should be interpreted as rate ratios instead of ORs.23
In these analyses, the ESI category was the dependent variable. ESI categories 4 and 5 were merged because of the small number of patients triaged in ESI category 5 and used as a reference category (n¼237). Besides WPSS and pain scores, other independent variables were gender, referrer, main complaint and age. The latter four variables were used in the analyses because in a previous study these appeared to be related to the ESI triage categories.24 The variable referrer consisted of patients referred by ambulance, a specialist, a general practitioner or patients who referred themselves to the ED. The variable main complaint was coded in accordance with the chapters of the International Classification of Diseases 10th edition (ICD 10), immediately after triage.25 It was decided to code main complaints this way to decrease the variability in ICD 10 codes, which was needed for the analyses. Univariate ordinal logistic regression analyses were performed and all variables which significantly (p#0.05) predicted urgency were selected for multivariate analysis. All analyses were performed using SPSS for Mac V.17.0.
RESULTS
In total, 929 patients presented at the ED during the study hours. Of these, 584 patients (62.9%) consented for participation and were included in the study. Of these, 40 patients had missing data (WPSS score (6.0%), pain score (1.0%) or age (0.3%)) and were excluded from the study, leaving 544 patients for further analyses. No significant differences (p¼0.53) were found between included and excluded patients, based on age and

The APACHE II

The APACHE II model was originally published in 1985 based on data from the US (Knaus et al,1985). It has been recalibrated twice for use in the UK, first following the Intensive Care Society’s APACHE II study in Britain and Ireland (Rowan, 1992; Rowan et al, 1993) and subsequently using data from the Case Mix Programme Database (Harrison et al, 2006). We regularly recalibrate the model using Case Mix Programme data to ensure that each critical care unit is being compared with current data. Coefficients from the most recent recalibration are used in the eDAR.

Risk predictions in APACHE II are based on:


 The APACHE II score – a score from 0 to 71 consisting of weights for age at admission to your unit (0 to 6 points) and severe conditions in the past medical history (0 to 5 points) plus an Acute Physiology Score (0 to 60 points) based on weightings for deviations from normal in the following twelve physiological parameters during the first 24 hours in the unit

o  temperature
o mean arterial pressure o heart rate
o  respiratory rate
o  A-aDO2 (if FiO2 ≥ 0.5) or PaO2 (if FiO2 < 0.5)
o arterial pH (or serum bicarbonate if no arterial blood gas recorded) o serum sodium

o  serum potassium
o serum creatinine (with double weighting for acute renal failure) o haematocrit (estimated from haemoglobin)
o  white blood cell count
o Glasgow Coma Score (assumed to be normal for patients sedated or paralysed and sedated for the whole of the first 24 hours in the unit, or for the entire stay if less than 24 hours)
 Admission directly from theatre following emergency surgery
 Diagnostic category (weightings for 58 non-surgical diagnoses and 50 surgical diagnoses, plus seven body systems, and a weighting for CPR within 24 hours prior to admission that overrides any other diagnostic category)

Exclusions


Admissions are excluded from the calculation of the APACHE II score if:
a. age at admission to your unit is less than 16 years; or
b. length of stay in your unit is less than 8 hours.

Additionally, admissions are excluded from the calculation of an APACHE II risk prediction if:
c. the admission is for primary burns;
d. the admission is following coronary artery bypass graft (CABG) surgery;
e. the admission is transferred in from another ICU; or
f. all twelve physiological variables are missing.

Readmissions of the same patient within the same hospital stay and admissions missing ultimate hospital outcome are excluded from comparisons of observed and expected mortality.

Guideline on The Management Of Acute Respiratory Distress Syndrome (ARDS) in Adult ICU

Aim and Scope
1)To ensure that all patients in ICU with ARDS are correctly identified and receive   the best evidence based treatment.
Definition
Onset of ARDS (diagnosis) must be acute, within 7 days of some defined event,  which may be sepsis, pneumonia, or simply a patient’s recognition of worsening  respiratory symptoms. (Most cases of ARDS occur within 72 hours of recognition of  the presumed trigger.)
Bilateral opacities consistent with pulmonary edema must be present but may be
detected on CT or chest X-ray. Ultrasound may also be used to define lung  pathology and the presence of non cardiogenic extra vascular lung water
Respiratory failure can be “not fully explained by cardiac failure or fluid overload,”
in the physician’s best estimation using available information.
ARDS Severity  PaO2/FiO2*  Mortality
()kpa
Mild 200 – 300 27%
(27 – 40)
Moderate 100 – 200 32%
(13-27)
Severe < 100 45%
(<13)
*on PEEP 5+ 
General Measures
1 All patients should have 100% compliance with the Ventilator Care  bundle
2 No chest physiotherapy unless as a trial to improve lobar collapse
3 Minimal suctioning via ETT
4 Normal feed as per protocol
5 Fluids. All patients will have a liberal fluid strategy during the initial resuscitation  phase (usually 0-48hours). If patients are then still vasopressor dependent, we will  aim to maintain a neutral fluid balance. Once inotropes are discontinued or are  being used in low doses to compensate for sedation, then we will aim to remove  the excess fluid that has been given. This will initially be performed using diuretics  but may require CVVHF if the fluid balance remains positive. Vasopressor may be  required to support the BP and  allow diuresis
6.     Ventilation
Mode: 1)VC SIMV  ( Volume control, synchronized mandatory ventilation)
           2) Volume assured PC SIMV (Pressure control, volume assured,  synchronized mandatory ventilation) This is not available on all ventilators
Settings: Peep 5-10cmH2O
               TV 6ml/kg ideal body weight.
               Plateau pressure < 30cmH20
               Rate: titrated to control PaCO2
Ideal body weight is calculated as follows:
Males        Length (in cm) – 100
Females   Length (in cm) – 105
The tidal volume required must be written every day at the top on the ICU  observation chart in red. It is the responsibility of the ICU consultant 1 to ensure that  this is done
7   All patients will have subglottic suction
The following patient group will be managed with an
extended ARDS care bundle
Diagnosis of ARDS as per above criteria
Ventilated for <36hours
A PaO2/FiO2 ratio<20kpa(150mmHg) for 12-24 hours on an FiO2 >0.6. 
NDMR
All patients who meet the above criteria  will be given a cisatracurium infusion. This  will be titrated to a train of four (TOF of 2 twitches). Paralyses will continue for as  long as they meet prone ventilation criteria.
Prone ventilation
All patients who do not have specific contraindications to prone ventilation will be  prone ventilated. They will be placed prone as per unit guidelines. They will remain  prone ventilated for at least 16 hours.

Prone ventilation will be stopped when any of the following criteria are met:
1) Improvement in oxygenation. This is defined as a Pao2:Fio2 ratio of ≥20, with a  PEEP of ≤10 cm of water and an Fio2 of ≤0.6. These criteria have to be sustained in  the supine position at least 4 hours after the end of the last prone session
2) A patient deteriorates compared to their PaO2:FiO2 ratio when supine
3) > 96 hours since first episode of prone ventilation
Management of a raised PaCO2
1) pH> 7.2 secondary to a respiratory acidosis will be tolerated
     The respiratory rate and not the tidal volume should be adjusted to help maintain  a    pH >7.2
2) If the pH remains less than 7.2  for >24 hours then consideration should be given  to using extra corporeal CO2 clearance
3) If the pH is < 7.1 for 4 hours or more with no other therapy (nebulisers etc)  available to reduce it, then extra corporeal CO2 clearance should be considered.
4) All patients being considered for extra corporeal CO2 clearance should initially  be discussed with our regional ECMO centre.
Management of a persistently low PaO2 (<8kpa)
1) Increase FiO2
2) Add nebulised prostacycline as per guideline
3) Maintain TV and peep
4) Discuss with regional ECMO centre
Recruitment maneuvers
1) All patients will have ‘inspiratory hold’ recruitment. This will be performed by  using the inspiratory hold function on the ventilators.
2) This will be 30cm H2O for 30 seconds
3) It should be performed after each disconnection or suctioning episode
4) It should be repeated as required when clinically it is felt that recruitment is  required.
5) It may be used as a trial to improve the PaO2

Steroids
All patients will be given methylprednisolone 0,5mg/kg/day (or equivalent) for 14  days unless contraindicated for standard reasons.
Documentation Control
Development of Policy: Consultation with: Approved by: Signature:
Print name and position: Date of Approval: Review Date:
References
            Dr James Low
Dr. Craig Morris, Dr. Nick Reynolds
ICU  Clinical Group
Nov 2013
Nov 2016
1) JAMA, June 2012 – Vol 307, No. 23
2) NEJM  June 2013 – Vol 368, No 23
3) NEJM  August 2001- Vol 345, No. 8
4) Crit Care Med. 2009 37(9):2680.

Manajemen cidera otak

Manajemen akut Trauma Cedera Otak

Manajemen cedera otak traumatis berfokus pada stabilisasi pasien dan pencegahan cedera saraf sekunder untuk menghindari kerugian lebih lanjut dari neuron. Penuh neuromonitoring termasuk tekanan intrakranial pengukuran jarang tersedia sebelum kedatangan pasien di unit perawatan intensif. Kerusakan saraf yang signifikan dapat terjadi antara saat cedera dan CT scan, pengukuran yang akurat dari ICP dan parameter lainnya. Manajemen akut pasien ini karena diarahkan dengan asumsi ada patologi intrakranial signifikan dan melembagakan langkah-langkah untuk melindungi jaringan otak hidup.

Penilaian

Penilaian cedera otak bergantung pada evaluasi Skor Glasgow Coma (GCS) dan pemeriksaan murid. Tradisional GCS di bawah 9 dianggap mencerminkan cedera otak parah. Namun dengan perbaikan dalam perawatan pra-rumah sakit dan pengetahuan yang lebih besar dari cedera otak, pasien tiba di departemen darurat sebelumnya dan cedera otak mereka masih dapat berkembang. Oleh karena itu langkah-langkah berikut harus dipertimbangkan dan porbably dilembagakan pada semua pasien dengan skor koma dari 12 atau di bawah.

Hipotensi akan mempengaruhi perfusi otak dan karena itu menurunkan Skor Koma Glasgow. Namun otak cedera manajemen harus dilembagakan atas dasar pemeriksaan awal dan tidak boleh ada penundaan untuk menilai apakah GCS membaik dengan resusitasi volume. Hal ini penting untuk mengidentifikasi tanda-tanda herniasi transtentorial yang akan datang karena ini akan mempengaruhi jalannya manajemen segera pasien ini. Hal ini diidentifikasi oleh sikap yang abnormal unilateral dan / atau adanya dilatasi pupil unilateral.

Serial penilaian adalah penting. Pasien mungkin tiba dengan GCS agak terganggu dan cepat memburuk akibat perluasan hematoma atau meningkatkan pembengkakan otak. Murid mungkin awalnya normal dan kemudian melebarkan sebagai kenaikan tekanan intrakranial dan otak mulai mengalami herniasi.

Pengelolaan

Tujuan spesifik dalam pengelolaan akut cedera otak traumatik parah adalah:

Melindungi jalan nafas & oksigenatVentilasi untuk normocapniahipovolemia yang benar dan hipotensiCT scan saat yang tepatBedah Saraf jika diindikasikanPerawatan Intensif untuk lebih lanjut monitoring dan manajemen

Hipoksia dan hipotensi adalah ancaman terbesar bagi hasil fungsional di cedera otak. Kontrol akut awal dari tiga parameter di atas mungkin memiliki dampak yang lebih dari semua langkah-langkah lain kemudian dipekerjakan. Hilangnya neuron progresif terjadi dari waktu cedera, bukan waktu kedatangan di rumah sakit. Cepat urut intubasi harus digunakan jika tersedia untuk mengamankan jalan napas dan maksimal mengoksidasi pasien. Hipovolemia dan hipotensi harus diperbaiki lebih awal dan mengambil prioritas di atas intervensi lain untuk cedera otak. Cedera lain yang menyebabkan perdarahan harus dibenahi pertama (atau secara bersamaan) sehingga memadai tekanan perfusi serebral dipertahankan. Pasien harus disimpan dibius untuk mencegah batuk atau Valsava manuver dari pertempuran ventilator, karena kenaikan ini tekanan intrakranial .

M salah satu intervensi yang digunakan dalam pengelolaan tekanan intrakranial mungkin memiliki efek yang merugikan pada resusitasi cardiopulmonary (misalnya. Manitol ) yang pada gilirannya akan memiliki efek yang merugikan pada perfusi serebral. Selain itu beberapa langkah dapat menjadi kontraproduktif bila digunakan tanpa pengawasan yang memadai (misalnya. Hiperventilasi ). Dengan demikian intervensi lebih lanjut digunakan tanpa bimbingan dari CT scan atau pemantauan ICP hanya ketika ada bukti herniasi yang akan datang otak (sikap unilateral dan / atau unilateral dilatasi pupil).

Sebuah CT scan otak harus diperoleh saat yang tepat, seperti yang ditentukan oleh kehadiran cedera lain dan gangguan fisiologis. Ini akan menggambarkan cedera otak dan menentukan apakah operasi diindikasikan untuk menghilangkan lesi intrakranial massa (epidural / subdural hematoma), dan tingkat cedera difus dan otak hadir pembengkakan.

Selama periode ini ada berpotensi melanjutkan iskemia otak dan kematian neuronal dan ketepatan waktu adalah esensi. Seharusnya tidak ada investigasi atau prosedur yang tidak perlu dan merusak teknik pengendalian harus digunakan sebagai diperlukan. Tidak ada tulang belakang atau panjang pencitraan tulang harus dilakukan sebelum CT scan investigasi ini tidak akan mempengaruhi manajemen pasien segera. Pasien hemodinamik tidak stabil harus memiliki investigasi minimum, kontrol perdarahan dengan sederhana berarti (operasi dan disingkat jika perlu) yang sesuai dan kemudian CT scan dan pengobatan cedera otak.

Jika ada tanda-tanda herniasi yang akan datang transtentorial (sikap unilateral dan / atau unilateral dilatasi pupil) atau jika ada yang cepat kerusakan neurologis progresif (tanpa sebab ekstrakranial), maka ada hipertensi intrakranial signifikan dan langkah-langkah harus diambil untuk mengendalikan ICP segera. Hiperventilasi harus dilembagakan untuk mengurangi PaCO 2 untuk tidak lebih rendah dari 3.5kPa (25mmHg) dan manitol harus diberikan sebagai bolus. Oksigenasi dan perfusi serebral harus dijaga. CT scan muncul, seperti operasi jika diindikasikan.

Jika ada luka lain yang mengarah ke perdarahan dan hipotensi ini masih diprioritaskan. Namun mungkin perlu untuk mempertimbangkan pengobatan cedera otak secara bersamaan dengan pengelolaan cedera ini (laparotomy atau torakotomi), bahkan tanpa CT scan untuk memandu terapi. lubang burr buta untuk mendeteksi koleksi ekstra-aksial mungkin tepat sebagai upaya terakhir dalam kasus ini.

trauma.org 5: 1 2000

Referensi

Chesnut RM, Marshall LF, Klauber MR et al. Peran cedera otak sekunder dalam menentukan hasil dari cedera kepala berat. J trauma 34: 216-222, 1993

Chesnut RM, Marshall SB, Piek J et al. Awal dan akhir hipotensi sistemik sebagai sumber sering dan fundamental iskemia serebral berikut cedera otak parah di Traumatic Coma Data Bank . Acta Neurochir Suppl (Wein) 59: 121-125, 1993

Bukit DA, Abraham KJ, West RH. Faktor-faktor yang mempengaruhi hasil dalam resusitasi pasien terluka parah. Aust NZ J Surg 63: 604-609, 1993

Jones PA, Andrews PJ, Midgley S et al. Mengukur beban penghinaan sekunder pada pasien cedera kepala selama perawatan intensif. J Neurosurg Anesthesiol 6: 4-14, 1994

Otak Trauma Foundation. Pedoman pengelolaan cedera kepala berat. 1995

Termal injuries/burns

  Thermal  Injuries/Burns

Ncbi prostalglandin journal

The  British  Burns  Association  has  identified  the  following  as  requiring  referral  to  a  burn  unit:
•  Burns > 10% of total body surface  area  (TBSA)  in  adults  (a  crude  calculation  may  be  made,   assuming  that  the  palm  of  the  patient’s  hand  is  equivalent  to  1%  of  total  body  surface)
•  Burns > 5% TBSA in children
•  Burns of special  areas,  eg  face,  hands,  feet,  genitalia  and  major  joints
•  Full thickness  burns  >  5%  TBSA
•  Electrical  and  chemical  burns
•  Burns associated  with  inhalation  injury
•  Circumferential  burns  of  the  limbs  or  chest
•  Burns in young children  or  the  elderly
•  Burn injuries  in  patients  with  pre-existing  medical  disorders  which  complicate  management,   prolong  recovery  or  effect  mortality
•  Suspected ‘non-accidental  injury’  (NAI).  

Superficial  Burns
a)    Description
Quick  capillary  return.  Red,  slightly  swollen  appearance.  No  blister  formation.  Any  damaged  epithelium may  peel  off  after  5  to  7  days  without  scarring.

b)  Treatment  Aim
•  To relieve pain
•  To protect from infection.

c)  Treatment
•  Immediately place  the  affected  part  under  cold  running  water  (approx  15°C)  for  at  least  20   minutes  (Yuan  et  al  2007). 

This  relieves  pain  and  reduces  the  temperature  of  the  burning process  
•  Remove any clothing  carefully  
•  Apply dressings  as  for  blisters.

Superficial,  Partial  Thickness  Skin  Loss  Burns
a)  Description
Slow  capillary  return.  Epidermis  and  superficial  layers  of  dermis  are  destroyed.  Hair  follicles, sebaceous  and  sweat  glands  are  intact.  This  is  likely  to  be  a  painful  burn  as  the  nerve  endings  have not  been  damaged.   Usually  heals  in  10  to  14  days,  without  scarring.

Deep,  Partial  Thickness  Skin  Loss  Burns a)  Description Slow  capillary  return.  Greater  part  of  the  dermis  is  lost.  Sensation  is  altered.  Patient  may  have  no  pinprick  sensation.

b)  Treatment  Aims  of  Both  Superficial  and  Deep Partial  Thickness  Skin  Loss  Burns
•  To relieve  pain
•  To protect  from  infection
•  To manage exudate. Reproduced  by  permission  of  NHS  Lothian c)  Treatment
•  Immediately place  the  affected  part  under  cold  running  water  (approx  15°C)  for  at  least  10  to  15   minutes  
•  Remove any clothing  carefully  avoiding  any  further  injury.
•  Apply non-adherent  interface  dressing  such  as  Atrauman®.  An  absorbent   secondary  dressing  such  as  polyurethane  foam  film  may  be  used. 

The  primary  dressing  may  be   left  in  place  and  the  secondary  dressing  changed  as  often    as  necessary,  depending  on  choice   of  product  and  exudate  levels. Note:    Silver  sulfadiazine  cream  should  not  be  used  routinely  until  after  specialist  assessment  as  this will  mask  the  wound  bed  and  make  for  difficult  assessment.

Full  Thickness  Skin  Loss  Burns
a)  Description
No  capillary  return. 
No  epithelium  so  burn  can  only  heal  by  contraction,  granulation  and  migration  of epithelium  from  wound  edges.  The  wound  may  look  pale,  charred  and  coagulated  veins  may  be visible.   
No  sensation  is  present  on  testing.  This  will  cause  scarring.

b)  Treatment  Aim
•  To protect from infection
•  To manage exudate.

c)  Initial  Treatment  and  Assessment
•  Immediately place  the  affected  part  under  cold  running  water  (approx  15°C)  for  at  least  10  to  15   minutes.  If  greater  than  3  hours  from  time  of  injury,  cold  water  will  have  no  beneficial  effect.
•  Remove any clothing  carefully  avoiding  any  further  injury.

d)  If  Patient  is  to  be  Transferred  to  Accident  &  Emergency  or  Burns  Unit
•  Cover all burned  areas  primarily  with  cling  film  (which  prevents  infection  and  allows  for  ease  of   assessment)  and  wrap  patient  in  clean  covers  to  prevent  heat  loss  
•  If transfer  journey  is  greater  than  2  to  3  hours,  a  secondary  surgical  absorbent  dressing  of   gauze  and  cotton  tissue  will  be  necessary  to  retain  exudates,  which  may  be  extensive. Note:    Silver  sulfadiazine  cream  should  not  be  used  until  after  specialist  assessment  as  this  will  mask the  wound  bed  and  make  for  difficult  assessment.  

f)  If  Patient  is  not  to  be  transferred
•            Apply primary non-adherent  interface  dressing  such  as  Atrauman®.   
•  Secondary dressings  should  be  highly  absorbent  whilst  maintaining  a  moist  wound  bed  as  thick   eschar  usually  forms.  This  may  be  debrided  surgically  or  by  autolysis.  
•  Treat as for wound type  as  it  progresses  through  wound  healing  stages.
•  Initially,  dressings  may  need  to  be  carried  out  daily  but  this  is  dependent  on  the  amount  of   exudate.
•  Argyll and Bute CHP patient  pathway  is  to  NHS  Greater  Glasgow  &  Clyde.    There  may,   therefore,  be  slight  differences  in  dressings  selection. More  information  is  available  from  the  following  website: http://www.cobis.scot.nhs.uk/

REFERENCE
Yuan  J,  Wu  C,  Holland  AJA,  Harvey  JG,  Martin  HCO,  La  Hei  ER,  Arbuckle  S,  Godfrey  C  (2007)  Assessment  of  cooling  on  an  acute scald  burn  injury  in  a  porcine  model.  J  Burn  Care  Res  28:  514–20.

Cavity wound

  Cavity  Wound

Description
A  wound  which  is  categorised  by  its  depth  and  tissue  involvement.  This  wound  type  may  be  acute  or chronic. Reproduced  by  permission  of  NHS  Lothian

Treatment  Aim
•  To  achieve  management  and  free  drainage of  exudate  
•  To protect  the  surrounding  skin
•  To prevent  infection
•  To remove necrosis  or  slough
•  To promote  granulation  from  the  base  of  the wound.
•  Treatment is dependent  on  the  position  of  the  wound  and  the  amount  of  exudate    (Dealey   2005).

Primary  Dressing  
•  Cavity fillers  e.g.  alginate  rope,  hydrofibre  rope,  

Secondary  Dressing  
•  Polyurethane foam film 19.4  Considerations
•  Rehydration  of  sloughy  wounds  may  increase  the  odour
•  Negative pressure  closure  may  be  indicated,  if  wound  exudate  or  depth  is  significant  (see   Specialist  Products  section)

REFERENCE
Dealey,  C.  (2005)  General  Principles  of  Wound  Management.  In:  The  Care  of  Wounds,d     3rd    edn.  Oxford:  Blackwell  Science.     30 

Necrotic wound

Necrotic  Wound

Description
Brownish/black,  dead  dehydrated  tissue,  leathery  in  texture.  May  be  hard  or  soft. When  an  area  of  tissue  becomes  ischaemic  for  any  length  of  time,  it  will  die.  The  area  may  form  a necrotic  eschar  or  scab. 

When  assessing  these  wounds  it  is  important  to  remember  that  the  wound may  be  more  extensive  than  is  apparent.  The  eschar,  or  slough,  masks  the  true  size  of  the  wound. Unless  necrotic  tissue  is  removed,  the  wound  will  continue  to  increase  in  size.  Intervention  is necessary  for  these  wounds  to  heal  (Dealey  2005). Reproduced  by  permission  of  NHS  Lothian

Treatment Primary  Dressing  
•  Hydrogel/sheet Secondary  Dressing  
•  Hydrocolloid  
•  Polyurethane  Foam  Film

Considerations
•  Debridement •  Wound will  deepen  as  necrosis  is  lifted

Treatment  Aim
•  To remove/debride  dead  tissue  
•  To rehydrate  the  wound.
•  Ischaemic  necrosis-Caution  with  rehydrating  these  wounds: 
Note:    Larval  therapy  is  not  appropriate  for  this  type  of  wound  until  the  necrosis  is  moist

REFERENCE
Dealey,  C.  (2005)  General  Principles  of  Wound  Management.  In:  The  Care  of  Wounds,  3nd  edn.  Oxford:  Blackwell  Science.

Sloughy wound

Sloughy  Wound

Description Viscous,  devitalised  tissue,  predominantly  yellow  in  colour.    It  is  most  often  found  as  patches  on  the wound  surface,  although  it  may  cover  large  areas  of  the  wound.  It  is  made  up  of  dead  cells  which  have accumulated  in  the  exudate.  (Dealey  2005). Reproduced  by  permission  of  NHS  Lothian

Treatment Dry  Slough

Treatment  Aim
•  To remove/debride  slough
•  To remove excess  exudate
•  To promote  autolysis.
•  The aim is to donate fluid  in  order  to  establish  a  moisture  balance  and  promote  autolysis.

Primary  Dressing    
•  Hydrogel/sheet

Secondary  Dressing  
•  Hydrocolloid Wet  Slough
•  The aim is to absorb fluid  in  order  to  establish  a  moisture  balance,  and  promote    autolysis.

Primary  Dressing  
•  Alginate or Fibrous  Hydrocolloid  (depending  on  the  levels  of  exudate)

Secondary  Dressing  
•  Polyurethane  Foam  Film

Considerations
•  larval  therapy  (see  specialist  products  section)
•  sharp  debridement  
•  monitoring  and  management  of  exudate  levels
•  when  using  a  product  that  donates  fluid  ensure  that  the  secondary  dressing  does  not  absorb  the   product  before  the  wound.  i.e.  gel  then  a  foam  product.

REFERENCE
Dealey,  C.  (2005)  General  Principles  of  Wound  Management.  In:  The  Care  of  Wounds,  3rd    edn.  Oxford:  Blackwell  Science. 

Over granulating wound

Over-Granulating Wound

Description 
Granulation tissue which is raised above the level of the surrounding skin. 

Treatment Aim 
• To reduce further development of granulation tissue
• To promote epithelialisation.  

Treatment  Primary Dressing 
• Polyurethane foam film, to provide uniform downwards pressure against the granulation  

Secondary Dressing 
• Only required if primary dressing is non-adherent  

 Considerations 
• Look for signs and symptoms of infection. Hyper-granulation can be encouraged by a bacterial   load.
• Trialling an antimicrobial applied with a secondary dressing that will provide uniform  downward pressure, as tolerated, on the wound may be of assistance.
• Topical steroids may be of use. Discuss with medical staff or nurse specialists in  your area.                                                               

Granulating wound

Granulating  Wound 

Description
Red,  granular  tissue. The  tops  of  the  capillary  loops  cause  the  surface  to  look  granular.  It  should  be  remembered  that  the walls  of  the  capillary  loops  are  very  thin  and  easily  damaged,  which  explains  why  these  wounds  bleed easily  (Dealey  2005). Reproduced  by  permission  of  NHS  Lothian

Treatment  Aim
•  To protect angiogenesis
•  To maintain moisture  balance.

Treatment Primary  Dressing
•  Alginate
•  Thin hydrocolloid
•  Hydrocolloid
•  Fibrous hydrocolloid
•  Polyurethane foam film  (depending  on  the  levels  of  exudate). Secondary  Dressing
•  Only required  if  primary  dressing  is  non-adherent   Considerations
•  Depending on the depth of  the  wound  cavity  packing  may  be  required.
•  If the wound is prone to bleeding,  alginates  can  be  useful  as  they  have  a  haemostatic  property.  

REFERENCE
Dealey,  C.  (2005)  General  Principles  of  Wound  Management.  In:  The  Care  of  Wounds,  3rd    edn.  Oxford:  Blackwell  Science.