scholarly journals Ischemic stroke induces cardiac dysfunction and alters transcriptome profile in mice

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Jie Chen ◽  
Jiahong Gong ◽  
Haili Chen ◽  
Xuqing Li ◽  
Li Wang ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Neurological Deficits ◽  
Heart Weight ◽  
Transcriptome Profile ◽  
Cross Sectional ◽  
Cardiac Atrophy ◽  
Extracellular Region ◽  
Transcriptome Response ◽  
Myocardial Atrophy ◽  
Tibia Length

Abstract Background Stroke can induce cardiac dysfunction in the absence of primary cardiac disease; however, the mechanisms underlying the interaction between the neurological deficits and the heart are poorly understood. The objective of this study was to investigate the effects of stroke on cardiac function and to identify the transcriptome characteristics of the heart. Results Stroke significantly decreased heart weight/tibia length ratio and cardiomyocyte cross-sectional areas and increased atrogin-1 and the E3 ubiquitin ligase MuRF-1, indicating myocardial atrophy in MCAO-induced mouse hearts. RNA sequencing of mRNA revealed 383 differentially expressed genes (DEGs) in MCAO myocardium, of which 221 were downregulated and 162 upregulated. Grouping of DEGs based on biological function and quantitative PCR validation indicated that suppressed immune response and collagen synthesis and altered activity of oxidoreductase, peptidase, and endopeptidase may be involved in MCAO-induced cardiomyopathy. The DEGs were mainly distributed in the membrane or extracellular region of cardiomyocytes and acted as potential mediators of stroke-induced cardiac dysregulation involved in cardiac atrophy. Conclusion Stroke induced a unique transcriptome response in the myocardium and resulted in immediate cardiac atrophy and dysfunction.

Abstract 526: Unraveling the Molecular Signature of Pregnancy Induced Hypertrophy

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Helen E Collins ◽  
Kyle Fulghum ◽  
Lindsey A McNally ◽  
Mallory L Foster ◽  
Kenneth Brittian ◽  
...  
Keyword(s):  
Late Pregnancy ◽  
Functional Adaptation ◽  
Molecular Signature ◽  
Heart Weight ◽  
Cardiomyocyte Hypertrophy ◽  
Molecular Processes ◽  
Cross Sectional ◽  
Lv Mass ◽  
Lv Volume ◽  
Tibia Length

Cardiovascular disease is the leading cause of death in pregnant and postpartum women. During pregnancy, the maternal heart rapidly adapts to the increasing physiological and metabolic demands of the growing fetus. This adaptation often takes the form of a physiological hypertrophy in which the maternal heart grows to increase cardiac output; however, the molecular processes underlying pregnancy-induced hypertrophy (PIH) are poorly understood. The goal of this study was to examine the transcriptomic and metabolic signatures associated with the structural and functional adaptations of the heart to pregnancy. Therefore, we performed timed pregnancy studies in 12-week-old female FVB/NJ mice, which were distributed into the following groups: non-pregnant control (NP; n = 14), mid-pregnancy (MP, 6d pregnant; n = 11), late-pregnancy (LP, 16d pregnant; n = 13), and 1-wk post birth (PB; n = 8). Heart weight to tibia length were higher in MP (7.77±1.02 mg/mm; p <0.05), LP (7.84±0.87 mg/mm; p <0.05), and PB mice (9.86±1.14 mg/mm; p <0.05) compared with NP mice (6.54±0.74 mg/mm). The sustained increase in PB heart weight was associated with increased myocyte cross sectional area, consistent with cardiomyocyte hypertrophy. Compared with NP hearts, echocardiographic measurements suggest significant increases in both end diastolic (36.0±5.1 vs 61.2±5.9 μl; p <0.05) and systolic LV volume (9.4±3.8 vs 21.0±1.4 μl; p <0.05) in PB hearts. These changes in PB hearts were associated with a significant increase in LV mass and a decline in ejection fraction. In LP and PB hearts, we also found higher expression of markers of hypertrophy ( Nppa, Nppb, Myh7 ). Subsequent RNA-seq analyses revealed enrichment in genes involved in cell proliferation, cytokinesis, and transcription in MP hearts; in metabolism genes in LP hearts; and in fibrotic and extracellular matrix genes in PB hearts. Together, these findings reveal the key molecular signature underlying the structural and functional adaptation of the heart during pregnancy and parturition, and may shed light on the molecular processes underlying PIH.

scholarly journals Ventricular TLR4 Levels Abrogate TLR2-Knockout-Mediated Adverse Cardiac Remodeling upon Pressure Overload in Mice

2021 ◽  
Vol 22 (21) ◽  
pp. 11823
Author(s):  
Elise L. Kessler ◽  
Jiong-Wei Wang ◽  
Bart Kok ◽  
Maike A. Brans ◽  
Angelique Nederlof ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Cardiac Remodeling ◽  
Pressure Overload ◽  
Heart Weight ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Cross Sectional ◽  
Tlr4 Mrna ◽  
Tibia Length

Involvement of the Toll-like receptor 4 (TLR4) in maladaptive cardiac remodeling and heart failure (HF) upon pressure overload has been studied extensively, but less is known about the role of TLR2. Interplay and redundancy of TLR4 with TLR2 have been reported in other organs but were not investigated during cardiac dysfunction. We explored whether TLR2 deficiency leads to less adverse cardiac remodeling upon chronic pressure overload and whether TLR2 and TLR4 additively contribute to this. We subjected 35 male C57BL/6J mice (wildtype (WT) or TLR2 knockout (KO)) to sham or transverse aortic constriction (TAC) surgery. After 12 weeks, echocardiography and electrocardiography were performed, and hearts were extracted for molecular and histological analysis. TLR2 deficiency (n = 14) was confirmed in all KO mice by PCR and resulted in less hypertrophy (heart weight to tibia length ratio (HW/TL), smaller cross-sectional cardiomyocyte area and decreased brain natriuretic peptide (BNP) mRNA expression, p < 0.05), increased contractility (QRS and QTc, p < 0.05), and less inflammation (e.g., interleukins 6 and 1β, p < 0.05) after TAC compared to WT animals (n = 11). Even though TLR2 KO TAC animals presented with lower levels of ventricular TLR4 mRNA than WT TAC animals (13.2 ± 0.8 vs. 16.6 ± 0.7 mg/mm, p < 0.01), TLR4 mRNA expression was increased in animals with the largest ventricular mass, highest hypertrophy, and lowest ejection fraction, leading to two distinct groups of TLR2 KO TAC animals with variations in cardiac remodeling. This variation, however, was not seen in WT TAC animals even though heart weight/tibia length correlated with expression of TLR4 in these animals (r = 0.078, p = 0.005). Our data suggest that TLR2 deficiency exacerbates adverse cardiac remodeling and that ventricular TLR2 and TLR4 additively contribute to adverse cardiac remodeling during chronic pressure overload. Therefore, both TLRs may be therapeutic targets to prevent or interfere in the underlying molecular processes.

Abstract 104: Protein Kinase GIα Functions in the Cardiac Myocyte as a Tonic Inhibitor of Pathologic Cardiac Hypertrophy In Vivo

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Robert M Blanton ◽  
James P Mendoza ◽  
Mark Aronovitz ◽  
David A Kass ◽  
Michael E Mendelsohn ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cardiac Hypertrophy ◽  
Cardiac Myocyte ◽  
Heart Weight ◽  
Cross Sectional ◽  
Lv Remodeling ◽  
Exon 1 ◽  
Tibia Length ◽  
Pathologic Cardiac Hypertrophy

Objectives: We and others previously demonstrated that activation of the NO-cGMP-Protein Kinase G (PKG) pathway inhibits cardiac hypertrophy and remodeling in vivo. However, it remains untested whether PKG specifically in the cardiac myocyte (CM) mediates these effects. We therefore tested the hypothesis that PKGIα inhibits pathologic cardiac hypertrophy through a specific role in the CM. Methods and Results: We created and characterized mice with CM-restricted excision of PKGIα. Mice were generated in which the PKGI exon 1 (specific for the Iα isoform) was flanked by loxP sites. We crossed these PKGIα fl/fl mice with αMHC-Cre mice which constitutively express Cre recombinase selectively in the CM. The resultant PKGIα fl/fl / αMHC-Cre+/- mice were compared with PKGIα fl/fl / αMHC-Cre-/- littermate controls (termed PKG CMKO and Ctrl, respectively). By age 3 months (n=5 per genotype), male PKG CMKO mice developed atrial and LV hypertrophy compared with Ctrl littermates PKG CMKO atrial weight/tibia length 0.33 ± 0.03 mg/mm vs 0.22 ± .01 in Ctrl, P <0.05; PKG CMKO LV/TL 5.0 ± 0.2 mg/mm vs 4.1 ± 0.4 in Ctrl, P <0.05). LV CM cross sectional area also increased in the 3 month old PKG CMKO mice (9445 ± 282 pixels PKG CMKO vs 8273 ± 213 in Ctrl, n>400 cells/genotype, 5 hearts per genotype; P <0.001). The systolic index end systolic elastance was decreased in 3 month old PKG CMKO mice (PKG CMKO 3.1 ± 0.4 mmHg/μ l vs 6.1 ± 1.0 in Ctrl-; P <0.05). Importantly, blood pressure did not differ between genotypes. By age 6 months, PKG CMKO mice developed early mortality (3 of 4 PKG CMKO males died at 6 months of age vs 0 of 4 Ctrl males). Total heart and atrial weights of male mice (n=3 PKG CMKO , 4 Ctrl) increased in PKG CMKO mice (heart weight/tibia length 10.8 ± 1.7 mg/mm in PKG CMKO vs 7.1 ± 0.6 in Ctrl; P <0.05; atrial weight/tibia length 2.3 ± 1.1 mg/mm in PKG CMKO vs 0.30 ± 0.1 Ctrl, P <0.05). LV fractional shortening percentage, recorded at 6 months age, trended lower in the PKG CMKO mice as well (35 ± 3% PKG CMKO vs 44 ± 4% Ctrl, P 0.09). Conclusions: These data provide the first evidence that PKGIα functions in the CM as a tonic inhibitor of age-dependent pathologic hypertrophy, supporting further study of PKGIα as a therapeutic target in the prevention and treatment of LV remodeling and congestive heart failure.

Abstract 36: Administration of 17β-Estradiol in C57Bl/6N Female Mice Leads to Cardiac Atrophy and Dysfunction via a β-Catenin Mechanism

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Georgios Kararigas ◽  
Laura C Zelarayan ◽  
Karl Toischer ◽  
Gerd Hasenfuss ◽  
Hubertus Jarry ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Structural Changes ◽  
Ring Finger ◽  
Pressure Overload ◽  
Heart Weight ◽  
Independent Manner ◽  
Cross Sectional ◽  
Hypertrophic Growth ◽  
Cardiac Atrophy ◽  
17Β Estradiol

The steroid hormone 17β-estradiol (E2) regulates several biological processes. In contrast to its anti-hypertrophic effects under pressure overload, we recently found that E2 induced physiological hypertrophic growth in healthy C57Bl/6J mice but not C57Bl/6N mice. Here, we aimed at the characterization of the effects of E2 in C57Bl/6N mice and tested the hypothesis that β-catenin mediates these E2 effects. Following ovariectomy, 2-month-old C57Bl/6N wild-type and cardiac-specific β-catenin-deleted (β-cat Δex2-6 ) mice were randomized to an E2-containing or soy-free (control, CON) diet ( n = 7-13/group). Cardiac function was examined by echocardiography following established procedures. The 3-month physiological dose of E2 led to a higher relative uterus weight compared with CON ( P < 0.001) in both WT and β-cat Δex2-6 mice. The relative heart weight was significantly reduced by E2 compared with CON in WT mice ( P < 0.001), while there was no significant effect in β-cat Δex2-6 mice. Cardiomyocyte cross-sectional area was also significantly decreased by E2 ( n = 5-7/group; P < 0.001) compared with CON in WT mice, while there was no significant effect in β-cat Δex2-6 mice. Echocardiography revealed a significant decrease in septum width ( P < 0.001) and posterior wall thickness ( P < 0.01) in E2 treated WT mice compared with CON, while there was no significant effect in β-cat Δex2-6 mice ( n = 8/group). These E2-induced structural changes in WT mice were accompanied by a significant decrease in cardiac function, namely a 23% decrease in fractional shortening compared with CON ( P < 0.05), while there was no significant effect in β-cat Δex2-6 mice. Immunoblotting revealed a significant increase in the levels of the ubiquitin ligase and key regulator of proteasome-dependent protein degradation muscle-specific RING finger protein 1 (MuRF1) by E2 compared with CON in WT mice ( P < 0.05), while there was no significant effect in β-cat Δex2-6 mice. Although we hypothesized increased autophagic activity, we found no effect on the autophagy-related protein LC3 in WT or β-cat Δex2-6 mice. In conclusion, our surprising findings show that E2 leads to cardiac atrophy and dysfunction in C57Bl/6N mice via a β-catenin mechanism seemingly in an autophagy-independent manner.

scholarly journals Functional capacity and mental state of patients undergoing cardiac surgery

2017 ◽  
Vol 30 (4) ◽  
pp. 805-811
Author(s):  
Bruna Corrêa ◽  
Dannuey Machado Cardoso
Keyword(s):  
Cardiac Surgery ◽  
Valve Replacement ◽  
Functional Capacity ◽  
Mental State ◽  
Myocardial Revascularization ◽  
Public Health Problem ◽  
Cross Sectional Study ◽  
Neurological Deficits ◽  
Cross Sectional ◽  
Duke Activity Status Index

Abstract Introduction: Cardiovascular diseases are a serious public health problem in Brazil. Myocardial revascularization surgery (MRS) as well as cardiac valve replacement and repair are procedures indicated to treat them. Thus, extracorporeal circulation (ECC) is still widely used in these surgeries, in which patients with long ECC times may have greater neurological deficits. Neurological damage resulting from MRS can have devastating consequences such as loss of independence and worsening of quality of life. Objective: To assess the effect of cardiac surgery on a patient’s mental state and functional capacity in both the pre- and postoperative periods. Methods: We conducted a cross-sectional study with convenience sampling of subjects undergoing MRS and valve replacement. Participants were administered the Mini-Mental State Exam (MMSE) and the Duke Activity Status Index (DASI) in the pre- and postoperative periods, as well as before their hospital discharge. Results: This study assessed nine patients (eight males) aged 62.4 ± 6.3 years with a BMI of 29.5 ± 2.3 kg/m2. There was a significant decrease in DASI scores and VO2 from preoperative to postoperative status (p = 0.003 and p = 0.003, respectively). Conclusion: This study revealed a loss of cognitive and exercise capacity after cardiac surgery. A larger sample however is needed to consolidate these findings.

Cardiac Manifestation among Patients with Hypothyroidism - A Cross-Sectional Study in North Karnataka

2021 ◽  
Vol 8 (26) ◽  
pp. 2283-2287
Author(s):  
Swetha Rajshekar Lakshetty ◽  
Nandini Devru
Keyword(s):  
Pericardial Effusion ◽  
Diastolic Dysfunction ◽  
Cardiac Dysfunction ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cross Sectional Study ◽  
Common Finding ◽  
Low Density ◽  
Sectional Study ◽  
Cross Sectional

BACKGROUND Hypothyroidism is the second most common endocrinopathy next to diabetes mellitus (DM). Hypothyroidism is associated with increased cardiovascular mortality and morbidity. Cardiovascular complications are some of the most profound, reproducible and reversible clinical findings associated with thyroid disease1 . Hence this study was undertaken to assess the cardiac dysfunction among patients with hypothyroidism by electrocardiogram (ECG) and echocardiogram (ECHO) so as to provide a proper treatment guideline even among milder cases. METHODS This was a cross sectional study carried among 50 new patients of hypothyroidism who presented to Navodaya Hospital, Raichur during 2015 to 2017. They were clinically evaluated and underwent relevant investigations, including thyroid profile estimation, cardiac evaluation using ECG and 2D ECHO. RESULTS Most cases fell in the age group of 31 - 40 years. There was an overall female preponderance (76 %) over all age groups with mean age of 42.02 years. Goiter was found in 8 % of patients, bradycardia and hypertension was seen in 30 % and 22 % respectively. Central nervous system (CNS) examination revealed delayed ankle jerk in 40 % followed by hoarseness of voice in 38 % of patients. Lipid analysis showed increase of total cholesterol (TC), low density lipoprotein (LDL), very low-density lipoprotein (VLDL), triglycerides (TGL) and decrease of highdensity lipoprotein (HDL). Normal ECG was found in 26 % of patients. Bradycardia was most common finding seen in 30 % (15) of patients. 24 % (12) of patients exhibited low voltage complexes. While, 46 % cases showed normal ECHO findings. 24 % of cases presented with pericardial effusion. 18 % cases presented with diastolic dysfunction among which majority were mild. None of the cases had severe diastolic dysfunction. Only a meagre 10 % cases showed intraventricular septum (IVS) thickness. CONCLUSIONS Pericardial effusion was seen among 24 % of patients while diastolic dysfunction was seen in 18 % patients. Thus, any unexplained pericardial effusion should be screened for hypothyroidism. KEYWORDS Hypothyroidism, Cardiac Dysfunction, 2D ECHO, ECG, Thyroid Stimulating Hormone (TSH)

scholarly journals Determinants of Timing of Presentation of Neurotrauma Patients to a Neurosurgical Center in a Developing Country

2018 ◽  
Vol 09 (04) ◽  
pp. 545-550 ◽  
Author(s):  
Toluyemi Adefolarin Malomo ◽  
Toyin Ayofe Oyemolade ◽  
Amos Olufemi Adeleye
Keyword(s):  
Primary Care ◽  
Primary Care Physicians ◽  
Late Presentation ◽  
Neurological Deficits ◽  
Delayed Presentation ◽  
Long Distance ◽  
College Hospital ◽  
Cross Sectional ◽  
Initial Care ◽  
Cord Injury

ABSTRACT Background: A major goal in neurotrauma management is the prevention of secondary neuronal injuries. This goal is time bound as neurological deficits once established are usually irreversible. Late presentation is the norm in most neurotrauma patients in developing countries. Aims: The aim of the study was to review the timing of presentation of neurotrauma patients and the possible causes of their late presentation for neurosurgical care in our practice. Methods: A cross-sectional study of a 4-month prospective database of neurotrauma patients presenting to the University College Hospital, Ibadan, was done. The participants’ biodata, injury characteristics, initial-care details before referral, and information on timing and causes of delay were analyzed. Results: The study subjects included 111 patients, 80.2% (89/111) were males, and 52.8% aged 21–40 years. Head injury (HI), spinal cord injury (SCI), and combined HI and SCI occurred, respectively, in 80.2%, 14.4%, and 5.4%. Road accidents followed by falls were seen in 73.9% and 14.4% (16), respectively. Just 46.8% (52/111) cases presented within 12 h of injury and only 37 (33.3%) within 4 h. Majority, 83.8% (93/111) were referrals from primary care. These referrals were delayed in 81.7% (76/93) of these. The referring health facilities were located intracity with our center in 54%. Other causes of delayed presentation of these study participants included long-distance travel to our center, lack of funds, or a combination of the above factors. Eighty-nine patients (80.2%) were brought in by family members and the remaining minority by passers-by and road safety personnel. Conclusions: Delayed referral from primary care features prominently in timing of presentation of neurotrauma patients in Nigeria. There is a need for collaboration as well as continuing medical education between the neurotrauma specialists and primary care physicians.

scholarly journals Korelasi Panjang Tulang Tibia Terhadap Tinggi Badan Pada Mahasiswa FK UMSU

2018 ◽  
Vol 1 (1) ◽  
pp. 1
Author(s):  
Putra Diandro Utama Ritonga ◽  
Hendra Sutysna
Keyword(s):  
Linear Regression ◽  
Body Height ◽  
Sampling Technique ◽  
The Body ◽  
Clinical Context ◽  
Exclusion Criteria ◽  
Cross Sectional ◽  
Regression Formula ◽  
Cross Sectional Design ◽  
Tibia Length

<p><strong><em>Introduction</em></strong><strong><em>:</em></strong><strong><em> </em></strong><em>Estimation of body height is one of the important parameter in the anthropology forensic, which the body height became the first action in identification. The regression formula using the tibia length, sex, and age might have valid approximation for body height which helpful in clinical context.</em><em> </em><em></em></p><p><strong><em>Methods</em></strong><strong><em>:</em></strong><strong><em> </em></strong><em>The analytic descriptive researchwith the cross-sectional design was done on 112 subject consist of male and female satisfy inclusion and exclusion criteria. Sample was selected by total sampling technique.</em><em></em></p><p><strong><em>Result</em></strong><strong><em>s: </em></strong><em>Tibia length resulting correlation ranging between 0,488 and 0,968 (p&lt;0,001). The</em><em> </em><em>linear regression formula showed Standard Error of the Estimate (SEE) ranging between 0,810 and 3,495 (p&lt;0,001).</em><strong><em> </em></strong><em></em></p><p><strong><em>Conclusion: </em></strong><em>A significant correlation between tibia length and body heightwas found with a strong correlation. Hence, a linear regression formula was derived for the estimation of body height from tibia length</em>.</p><p><strong>Keywords</strong>: tibia length; body height; regression formula; anthropometry</p>

scholarly journals Microalbuminuria in Ischaemic Stroke and its Relationship with Neurological Defects

2010 ◽  
Vol 15 (Number 2) ◽  
pp. 15-18
Author(s):  
S S Chowdhury ◽  
T Mehdi ◽  
F Alam ◽  
R Ishrat ◽  
S Parveen ◽  
...  
Keyword(s):  
Risk Factors ◽  
Ischaemic Stroke ◽  
Developed Countries ◽  
Cross Sectional Study ◽  
Neurological Deficits ◽  
Sectional Study ◽  
Cross Sectional ◽  
Common Cause ◽  
Face To Face ◽  
Structured Questionnaire

Stroke is Me third common cause of death in developed countries. Ischaernic stroke accounts for about 83 percent of all cases. For ischaemic stroke, besides modifiable and nononodifiable risk factors. there are some potential nosy risk factors which include mieroalbuminuria. Site objective of this study was to observe the association of microalbuminuria with isehaemic stroke and as well as consequent neurological deficits. This cross sectional study was done among 100 diagnosed patients of ischaeoric stroke of both sexes. A structured questionnaire and checklist was used to collect data through face to face interview. Urinary microalbuminuria was mesured in all study subjects and assessment of necrological defects was done by modified Ranakin scale. The study revealed that the frequency of presence of microallmminteria was significantly high in ischaernic stroke. Higher the level of mieroalburninuria higher was the necrological deficit. So, microalbunrinuria may be a marker for the process to develop the ischamnic stroke.

scholarly journals Efektivitas Alih Baring Tiap 2 Jam Terhadap Pencegahan Ulkus Dekubitus pada Pasien Pasca Stroke dengan Tirah Baring Lama di Bangsal Saraf RSUD Arifin Achmad Pekanbaru

2017 ◽  
Vol 4 (2) ◽  
pp. 133
Author(s):  
Bevi Dewi Citra ◽  
Hermes C. Sitompul ◽  
Tuti Restuastuti
Keyword(s):  
Intervention Study ◽  
Preventive Intervention ◽  
Decubitus Ulcer ◽  
Medical Rehabilitation ◽  
Neurological Deficits ◽  
Stroke Patients ◽  
Cross Sectional ◽  
Post Stroke ◽  
Rehabilitation Programs ◽  
Significant Difference

Neurological deficits on stroke patients can caused immobility. Decubitus ulcer is one of immobilty’s complication.Two hours repositioning is one of medical rehabilitation programs in decubitus prevention. The aim of this study is todescribe effectiveness of two hours repositioning to prevent decubitus ulcer, especially on post-stroke patients. Thisstudy was a preventive intervention study with cross-sectional approach. Sample consists of 32 patients. Group Iconsists of 16 patients with repositioning intervention. On the otherhand, group II consists of 16 patients withoutrepositioning intervention. Then, this two groups were compared and were looked for the effectiveness. from thisstudy, we knew that prevalence of decubitus ulcer on post-stroke patients are 19.4% with the effectiveness of two hoursrepositioning is 87.5%. There was significant difference between these two groups to prevent decubitus. it occurred ongeriatric patients with percentage of 75%. Its Proportion for female: male are 2:1. It is commonly occurred on firstweek hospitalization, especially grade 2 (33.3%). It is mostly located on sacrum (100%).

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