How does warfarin use affect intracerebral hematoma volume. What are the key factors influencing hematoma size in ICH patients. Does INR level correlate with increased hematoma volume. What are the implications for patient care and mortality rates.

The Relationship Between Warfarin Use and Intracerebral Hematoma Volume

Intracerebral hemorrhage (ICH) is a severe form of stroke with high mortality rates. Recent studies have shown that patients using warfarin, a common anticoagulant, at the time of ICH onset have poorer outcomes. This article explores the connection between warfarin use and initial hematoma volume, a critical factor in ICH prognosis.

A retrospective study analyzed 258 ICH patients, including 51 on warfarin therapy, to investigate whether warfarin use correlates with larger initial hematoma volumes. The research aimed to understand the mechanism by which warfarin worsens ICH outcomes, given that anticoagulant-associated ICH (AAICH) now accounts for approximately 20% of all ICH cases.

The Impact of INR Levels on Hematoma Size

International Normalized Ratio (INR) is a measure of blood clotting time and is used to monitor warfarin therapy. The study revealed a nuanced relationship between INR levels and hematoma volume:

• INR <1.2: Average hematoma volume of 13.4 mL
• INR 1.2-2.0: Average hematoma volume of 9.3 mL
• INR 2.1-3.0: Average hematoma volume of 14.0 mL
• INR >3.0: Average hematoma volume of 33.2 mL

Notably, patients with an INR >3.0 had significantly larger hematoma volumes compared to those with lower INR values. This finding suggests that while warfarin use generally increases hematoma size, the effect is most pronounced in patients with INR levels exceeding the typical therapeutic range.

Key Predictors of Larger Hematoma Size in ICH Patients

The study identified several factors associated with increased hematoma volume:

1. INR >3.0
2. ICH location (lobar compared to deep cerebral)
3. Shorter time from stroke onset to brain scan

Understanding these predictors can help healthcare providers assess the potential severity of ICH cases more accurately and tailor treatment strategies accordingly.

The Role of Warfarin in ICH Mortality Rates

Previous research has established that warfarin use at ICH onset is an independent predictor of mortality. The current study suggests that the larger initial hematoma volumes observed in warfarin users, particularly those with INR >3.0, likely contribute significantly to this increased mortality risk.

Do larger hematomas fully explain the excess mortality in warfarin users with ICH? While hematoma size is a crucial factor, other aspects such as hematoma expansion after initial presentation and the frequency of intraventricular hemorrhage (IVH) may also play roles in the poorer outcomes observed in this patient group.

Implications for ICH Management and Treatment Strategies

The findings of this study have important implications for the management of ICH patients, especially those on warfarin therapy:

• Rapid INR assessment upon hospital admission
• Prioritization of immediate warfarin reversal in patients with elevated INR
• Close monitoring of patients with INR >3.0 due to increased risk of larger hematomas
• Development of strategies to prevent INR levels from exceeding the therapeutic range in warfarin users

Can early intervention to reverse warfarin’s effects improve outcomes in ICH patients? While this study doesn’t directly address this question, the correlation between high INR and larger hematoma volumes suggests that prompt reversal of anticoagulation could potentially limit hematoma growth and improve patient prognosis.

Limitations and Future Research Directions

While this study provides valuable insights into the relationship between warfarin use and ICH severity, several limitations and areas for future research emerge:

• The retrospective nature of the study limits causal inferences
• The sample size, particularly of warfarin users, is relatively small
• The study does not address the impact of newer anticoagulants on ICH volume
• Further investigation is needed on the effectiveness of rapid warfarin reversal in improving outcomes

Future studies should aim to address these limitations and explore additional factors that may influence ICH severity and outcomes in anticoagulated patients.

The Evolving Landscape of Anticoagulation and ICH Risk

As the use of anticoagulants continues to rise, particularly in aging populations, understanding their impact on ICH becomes increasingly crucial. This study highlights the complex relationship between warfarin use, INR levels, and hematoma volume, providing valuable insights for clinical practice.

How might the findings of this study influence anticoagulation management in high-risk patients? Healthcare providers may need to reassess the risk-benefit ratio of warfarin therapy, especially in patients prone to INR fluctuations. Additionally, more frequent INR monitoring and stricter control might be warranted to minimize the risk of severe ICH in warfarin users.

Emerging Alternatives to Warfarin

The challenges associated with warfarin use in ICH patients underscore the importance of researching alternative anticoagulants. Novel oral anticoagulants (NOACs) have emerged as potential alternatives, offering more predictable pharmacokinetics and potentially lower risks of intracranial bleeding.

Do NOACs offer a safer anticoagulation option for patients at risk of ICH? While initial studies suggest that NOACs may have a more favorable safety profile regarding intracranial bleeding, more research is needed to fully understand their impact on ICH volume and outcomes in comparison to warfarin.

Optimizing ICH Care: A Multifaceted Approach

The findings of this study emphasize the need for a comprehensive approach to ICH management, particularly in anticoagulated patients. Key elements of optimized care may include:

• Rapid assessment and imaging upon hospital arrival
• Immediate reversal of anticoagulation in appropriate cases
• Close monitoring for hematoma expansion
• Tailored treatment strategies based on ICH location and initial volume
• Careful consideration of anticoagulation resumption post-ICH

Can improved protocols for managing anticoagulated ICH patients significantly reduce mortality rates? While more research is needed, the strong correlation between INR levels, hematoma volume, and mortality suggests that optimized management strategies could potentially improve outcomes in this high-risk group.

The Role of Neuroimaging in ICH Management

Advanced neuroimaging techniques play a crucial role in the assessment and management of ICH patients. The study’s finding that shorter time from stroke onset to scan was associated with larger hematoma volumes underscores the importance of rapid imaging in acute stroke care.

How can healthcare systems optimize their stroke protocols to minimize delays in neuroimaging? Potential strategies include:

• Implementation of mobile stroke units equipped with CT scanners
• Streamlined in-hospital workflows to expedite imaging
• Use of artificial intelligence for rapid image analysis and decision support
• Telemedicine solutions to provide expert interpretation in remote settings

Public Health Implications and Prevention Strategies

The increasing prevalence of AAICH highlights the need for public health initiatives aimed at preventing and managing ICH in anticoagulated patients. Key areas of focus may include:

1. Education programs for patients on warfarin about the importance of regular INR monitoring
2. Development of community-based anticoagulation clinics to improve INR control
3. Implementation of risk stratification tools to identify patients at highest risk of ICH
4. Research into genetic factors that may predispose individuals to warfarin-associated ICH

Could targeted interventions for high-risk warfarin users reduce the incidence of severe ICH? While challenging to implement, personalized approaches to anticoagulation management based on individual risk factors and genetic profiles may hold promise in minimizing ICH risk while maintaining effective anticoagulation.

The Economic Burden of Warfarin-Associated ICH

Beyond the clinical implications, warfarin-associated ICH poses a significant economic burden on healthcare systems. Larger hematoma volumes are associated with increased length of hospital stay, higher rates of long-term disability, and greater healthcare costs.

How can healthcare systems balance the cost-effectiveness of warfarin therapy with the potential economic impact of severe ICH? Considerations may include:

• Cost-benefit analyses of warfarin versus newer anticoagulants
• Investment in prevention strategies and optimized management protocols
• Development of risk prediction models to guide anticoagulation choices
• Exploration of value-based care models for anticoagulation management

By addressing these economic considerations alongside clinical factors, healthcare systems can work towards more sustainable and effective approaches to anticoagulation therapy and ICH management.

Warfarin use leads to larger intracerebral hematomas

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• PMC2668872

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Neurology. 2008 Sep 30; 71(14): 1084–1089.

doi: 10.1212/01.wnl.0000326895.58992.27

PMCID: PMC2668872

NIHMSID: NIHMS93125

PMID: 18824672

M L. Flaherty, MD, H Tao, PhD, M Haverbusch, BSN, P Sekar, MS, D Kleindorfer, MD, B Kissela, MD, P Khatri, MD, B Stettler, MD, O Adeoye, MD, C J. Moomaw, PhD, J P. Broderick, MD, and D Woo, MD

Author information Copyright and License information Disclaimer

Background:

Among patients with intracerebral hemorrhage (ICH), warfarin use before onset leads to greater mortality. In a retrospective study, we sought to determine whether warfarin use is associated with larger initial hematoma volume, one determinant of mortality after ICH.

Methods:

We identified all patients hospitalized with ICH in the Greater Cincinnati region from January through December 2005. ICH volumes were measured on the first available brain scan by using the abc/2 method. Univariable analyses and a multivariable generalized linear model were used to determine whether international normalized ratio (INR) influenced initial ICH volume after adjusting for other factors, including age, race, sex, antiplatelet use, hemorrhage location, and time from stroke onset to scan.

Results:

There were 258 patients with ICH, including 51 patients taking warfarin. In univariable comparison, when INR was stratified, there was a trend toward a difference in hematoma volume by INR category (INR <1.2, 13.4 mL; INR 1.2–2.0, 9.3 mL; INR 2.1–3.0, 14.0 mL; INR >3.0, 33.2 mL; p = 0. 10). In the model, compared with patients with INR <1.2, there was no difference in hematoma size for patients with INR 1.2–2.0 (p = 0.25) or INR 2.1–3.0 (p = 0.36), but patients with INR >3.0 had greater hematoma volume (p = 0.02). Other predictors of larger hematoma size were ICH location (lobar compared with deep cerebral, p = 0.02) and shorter time from stroke onset to scan (p < 0.001).

Conclusion:

Warfarin use was associated with larger initial intracerebral hemorrhage (ICH) volume, but this effect was only observed for INR values >3.0. Larger ICH volume among warfarin users likely accounts for part of the excess mortality in this group.

GLOSSARY

AAICH

= anticoagulant-associated intracerebral hemorrhage;

GERFHS

= Genetic and Environmental Risk Factors for Hemorrhagic Stroke;

HR

= hazard ratio;

ICH

= intracerebral hemorrhage;

INR

= international normalized ratio;

IVH

= intraventricular hemorrhage.

Warfarin use at the onset of intracerebral hemorrhage (ICH) is an independent predictor of mortality among ICH patients.^1,2 Understanding the mechanism by which warfarin worsens ICH outcome is important because anticoagulant-associated intracerebral hemorrhage (AAICH) has become more common in the past two decades and now accounts for approximately 20% of all ICH.^1,3

Among the factors influencing ICH outcome, hematoma volume at presentation to medical care, intraventricular extension of hemorrhage, and hematoma expansion after presentation are important variables that could be influenced by warfarin use. If hematoma expansion after presentation to medical care is a major cause of morbidity and mortality among AAICH patients, agents that promote rapid hemostasis and prompt reversal of coagulopathy could improve outcome. However, if the majority of excess mortality associated with warfarin use is caused by larger hematomas or more frequent intraventricular hemorrhage (IVH) at presentation, these therapies may be less effective because the window for intervention has passed.

Studies of the effect of warfarin on ICH volume to date have generally been small or referral based and have provided conflicting results.^4–8 We sought to determine 1) the predictors of initial hematoma volume among patients with ICH in a large population-based stroke study and 2) the relationship of INR and initial hematoma volume.

This article analyzes a group of patients with ICH ascertained as part of the Genetic and Environmental Risk Factors for Hemorrhagic Stroke (GERFHS) study. The methodology of the GERFHS study has been previously described.⁹ The institutional review board for each participating hospital system approved the GERFHS study.

For this report, we attempted to ascertain all persons aged ≥18 years from the five-county Greater Cincinnati/Northern Kentucky area who were hospitalized with ICH between January 1 and December 31, 2005. Cases were identified by retrospective review of primary and secondary International Classification of Diseases, 9th Revision, codes 430 through 438. 9. Study nurses also maintained active surveillance (“hot pursuit”) at several hospitals that treat most ICH in the area by reviewing neurosurgery logs and patient rosters several times each week.⁹ All potential cases were abstracted by study nurses and reviewed in detail by study physicians. Patients living outside the five counties of interest were excluded from this analysis by zip code of residence. Other exclusion criteria were previous ICH, traumatic ICH, hemorrhagic cerebral infarction, and hemorrhage associated with brain tumor, encephalitis, recent endarterectomy, and thrombolytic treatment of ischemic stroke. Patient demographics and putative risk factors for ICH, including warfarin and antiplatelet drug use before stroke onset, were recorded by chart review. The first available international normalized ratio (INR) value upon medical presentation was recorded. For all patients, the first available CT or MRI scan was reviewed.

Radiographs were reviewed by one of two authors (H. T. or M.L.F.). Hemorrhage volumes were measured by using the abc/2 method.¹⁰ IVH was not included in volume calculations. The intraclass correlation for hemorrhage volume was tested for 31 scans and was found to be 0.97 for the difference between the two reviewers. The degree of IVH was documented by using an ordinal scale described by Graeb, where the amount of blood in each ventricle is determined and the scores from each ventricle are summed.^11–13 The intraclass correlation for IVH score was again tested for 31 scans and was found to be 0.99 for the difference between the two reviewers.

Hematoma volumes were log transformed to approximate normality. To identify potential predictors of initial hematoma volume, univariable analyses for categorical variables were performed by using t tests or analysis of variance as appropriate. The continuous variables of age and time from stroke onset to first scan were tested with a general linear model. Tested categorical variables are presented in . Patients were both dichotomized as using or not using warfarin and were stratified by INR level (INR <1.2, 1.2–2.0, 2.1–3.0, >3.0).

Table 1 Univariable analyses of initial hematoma volume

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A multivariable generalized linear model was constructed to determine whether INR influenced ICH volume after adjusting for other factors. Variables from with p < 0.20 were included in the multivariable model and backward eliminated to a significance level of p <0.10. Age (p = 0.013) and stroke onset to scan time (p = 0.001) were also significant in univariable analysis and were included in the multivariable model. Warfarin use was not included in the multivariable model because of colinearity between the stratified INR values and the dichotomized warfarin variable. The referent values in the multivariable model were deep cerebral location, INR <1.2, and initial scan 2 hours after stroke onset.

The relationship between warfarin use and IVH was tested by using warfarin as a dichotomized variable and also by stratifying INR (<1.2, 1.2–2.0, 2.1–3.0, >3.0). This association was tested by using both IVH as a dichotomized variable (“yes” or “no”) and using the full spectrum of IVH scores via ordinal logistic regression.

To better understand the effect of INR on outcome after ICH, we analyzed the relationships between clinical and radiographic variables and 90-day mortality. Variables tested in univariable analysis were age, race, sex, history of diabetes, history of hypertension, history of heart disease, antiplatelet drug use, presence of IVH, location of hemorrhage, volume of hemorrhage, baseline Glasgow Coma Scale score, and INR stratified as <1.2 (referent), 1.2–2.0, 2.1–3.0, and >3.0. Variables with p <0.20 in univariable analysis were entered into a Cox proportional hazards model, and variables with p > 0.10 were then backward eliminated from this model.

There were 277 patients with ICH between January 1 and December 31, 2005, who met study criteria. After exclusion of 8 patients whose hemorrhages occurred while they were using heparin or low-molecular-weight heparin without concomitant warfarin use, 6 patients with pure IVH, and 5 patients who were not of black or white race, there were 258 patients with ICH (51 taking warfarin) remaining for analysis. Initial imaging was a CT scan for 256 of 258 patients. The mean age was 68.5 years (SD 16.4 years). The mean time from stroke onset to first scan was 14.5 hours (SD 30.6 hours). The median time from stroke onset to first scan was 4.7 hours. There were 22 patients without INR results. Because none of these patients were taking warfarin or other anticoagulants, they were assigned INR values of 1.0. The mean INR was 3.1 (SD 2.0) for warfarin users, compared with 1.1 (SD 0.2) among other patients (p < 0.001). The median INR was 2.7 for warfarin users and 1.0 for other patients. Among warfarin users, 2 (4%) had INR levels <1.2, 14 (27%) had INR values of 1.2–2.0, 18 (35%) had INR values of 2.1–3.0, and 17 (33%) had INR values >3.0. Among patients not documented to be taking warfarin, 175 (85%) had INR values <1.2, 29 (14%) had INR values of 1.2–2.0, 3 (1%) had INR values of 2.1–3.0, and 0 had INR values >3.0. Of all patients, 107 (41%) had some degree of IVH.

Univariable analyses for hematoma volume are presented in . When INR was stratified, there was a trend toward a difference in hematoma volumes by INR category (p = 0.10). When patients were dichotomized according to warfarin use, patients taking warfarin had larger hematomas than those not taking warfarin (p = 0.03). Increasing systolic blood pressure (p = 0.003) and increasing glucose levels (p = 0.005) at presentation were both associated with larger hematoma size in univariable analysis, but these variables were not included in our multivariable model because we were uncertain whether their relationship to hematoma size was cause or effect.

The multivariable generalized linear model is presented in . Compared with patients with INR <1.2, there was no difference in hematoma size for patients with INR 1.2–2.0 (p = 0.25) or INR 2.1–3.0 (p = 0.36), but patients with INR >3.0 had greater hematoma volume (p = 0.02). When patients with INR 1.2–3.0 who were not taking warfarin were excluded from the analysis, the mean hematoma volume in the INR 1.2–3.0 group increased, but results of the multivariable model were similar. As an example of the effect of anticoagulation, the expected hematoma volume of a deep cerebral ICH with INR <1.2 and CT scan 2 hours after stroke onset is 15.33 mL. The expected volume of a deep cerebral ICH with INR >3.0 imaged 2 hours after onset is 15.33 mL × 2.64 = 40.47 mL. The effect of INR in this instance is illustrated in the , which shows hemorrhages of 15 and 40 mL.

Table 2 Multivariable generalized linear model of initial hematoma volume

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Figure Comparison of 15- and 40-mL intracerebral hematomas

CT scans from 15-mL (A) and 40-mL (B) deep cerebral intracerebral hemorrhages (ICHs). This approximates the difference between an ICH with an international normalized ratio (INR) <1.2 and an ICH with an INR >3.0 as seen in the multivariable generalized linear model.

We also modeled hematoma volume (nontransformed) against the actual INR values and a second-order term (square of INR) to examine whether the relationship between hematoma volume and INR was nonlinear. We used all the other factors that were previously included in the multivariable model and backward eliminated to include only those that had p <0.10. The p values for the linear term and the quadratic term for INR were 0.002 and 0.02. This suggests that the volume of hemorrhage was nonlinearly related to the INR.

Other factors that independently predicted larger hematoma size were lobar location (p = 0.02) and shorter time from stroke onset to scan (p <0.001). Antiplatelet drug use showed a trend toward association with larger hematoma volume in univariable analysis but fell out of multivariable analysis. When forced into the final model, the p value for antiplatelet drug use was 0.36.

In univariable analysis, warfarin users were not more likely to have IVH than other patients (45% vs 41%; p = 0.58). There was no association between warfarin use and degree of IVH as measured by the Graeb scale (p = 0.72), or between stratified INR values and the presence or degree of IVH.

The relationships between INR strata and 90-day mortality after ICH are presented in . In both univariable and multivariable analyses, compared with INR <1.2, initial INR of 1.2–2.0 was not associated with worse outcome, while INR of 2.1–3.0 and INR >3.0 were associated with worse outcome. Multivariable analyses are presented with and without initial hemorrhage volume included in the model. The INR stratum of >3.0 conferred the highest point estimate of risk in univariable analysis. This effect was attenuated in multivariable analyses, especially when volume was included in the model.

Table 3 Relationships between INR and mortality after ICH

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Warfarin anticoagulation is increasingly relevant to the care of patients with ICH.³ During 2005, nearly 20% of patients with ICH in Greater Cincinnati were taking warfarin, with a much smaller number receiving heparin anticoagulation. Mortality is increased for AAICH patients. In Greater Cincinnati from 1998 to 2003, the 1-day mortality rate among AAICH patients was 33%, compared with 16% for ICH patients without coagulopathy.¹⁴ This mortality gap remained constant through 1 year.

Patients with AAICH are on average older and have more medical comorbidities than other ICH patients, factors that likely contribute to worse outcomes.¹⁴ In addition to these factors, three important influences on outcome after ICH that may be affected by warfarin use are initial hematoma volume, IVH, and hematoma growth.

Hematoma growth has received considerable attention as a target for therapeutic intervention using ultra-early hemostatic therapy. ^15,16 Although prospective data are lacking, small retrospective studies suggest that warfarin-associated ICH is more likely to expand and expand for a longer duration than ICH without coagulopathy.^8,17 Ultra-early hemostatic therapy and rapid reversal of anticoagulation are therefore attractive targets for improving outcome after AAICH.

Our study found that warfarin anticoagulation with INR values >3.0 was associated with larger initial hematoma volumes. This association and the finding of a nonlinear relationship between hematoma volume and INR suggest there may be a threshold for the effect of INR on hematoma volume. However, interpretations should be tempered by the relatively small numbers of patients in our upper INR strata. Confirmation of our results in another population-based study of ICH patients would be helpful.

Although hemostasis and anticoagulant reversal remain important targets to improve outcome among AAICH patients, our findings indicate that some of the excess mortality among AAICH patients will not be remediable by these strategies. In a recently published multivariable model of ICH outcome among 218 patients without coagulopathy, for each 1.0-mL increase in baseline hematoma volume, the hazard ratio for death increased by 1%.¹⁸ When modeling hematoma size in our population, patients with INR >3.0 had initial hematoma volumes approximately 25 mL greater than those of patients without coagulopathy, enough to produce a potent effect on mortality in this group. Subjects with INR of 2.1–3.0 had greater risk of death but did not have larger initial hematomas than subject with lower INR, indicating that hematoma expansion or medical comorbidities likely contribute to mortality for subjects with INR >2.0. Again, because of relatively small numbers in the higher INR strata, replication in an independent, population-based data set would help substantiate these findings.

Intraventricular hemorrhage is an additional factor that leads to poor outcome after ICH. Both IVH at presentation and growth of IVH over time have been reported to negatively affect prognosis. ¹⁹ We did not find an effect of warfarin on initial presence or severity of IVH, but we cannot exclude the possibility that warfarin produces more IVH growth with time.

Some studies have found antiplatelet drug use to be an independent predictor of death after ICH,^20,21 whereas others have not.^2,22,23 Our data do not show an association between antiplatelet use and initial hematoma volume. This indicates that an adverse effect of antiplatelet use on survival, if present, is due to another mechanism. The larger size of lobar hemorrhages relative to deep cerebral hemorrhages has been reported. However, deep cerebral ICH is more likely to rupture into the ventricular system than is lobar ICH.^24,25 These counterbalancing influences may explain why prognoses after lobar ICH and deep cerebral ICH are similar.¹ Finally, patients with larger and more devastating ICH are likely to present to the emergency department more rapidly, explaining the relationship between onset to scan time and initial hematoma volume.

Our study is limited by its retrospective nature. However, it is strengthened by our population-based case ascertainment, which includes patients receiving only one brain scan, patients not referred to tertiary centers, and patients receiving comfort care after diagnosis. We do not have data on the timing of anticoagulant reversal. INR testing was likely undertaken before the initiation of reversal in most cases. Patients who had their warfarin reversed before a blood draw for INR may have partially confounded our results. We did not review all scans subsequent to emergency department presentation for all patients. Therefore, we cannot determine whether warfarin-related hemorrhages expand or rupture into the ventricles more frequently than other hematomas do after initial presentation, nor can we estimate the potential benefit of hemostatic therapy in this setting. Ideally, a prospective study will be undertaken that includes all ICH patients in a defined population and obtains standardized, serial scans over time, allowing comparison of the natural history of ICH with and without anticoagulant use.

Statistical analyses were performed by P.S.

Address correspondence and reprint requests to Dr. Matthew L. Flaherty, Department of Neurology, University of Cincinnati Academic Health Center, 260 Stetson St., Room 2316, PO Box 670525, Cincinnati, OH 45267-0525 [email protected]

Supported in part by the National Institute of Neurological Disorder and Stroke (R-01-NS 36695) and a University of Cincinnati College of Medicine Medical Student Summer Research Fellowship.

Disclosure: M.L.F. has received compensation for activities with Novo Nordisk and provided a grand rounds presentation sponsored by an unrestricted educational grant from PhotoThera, Inc. J.P.B. has received compensation for activities with Ono Pharmaceuticals, Novo Nordisk, and Boehringer-Ingelheim. He was a member of the steering committee for trials of activated recombinant factor VII for treatment of acute intracerebral hemorrhage. He has received financial support/grant support from EKOS Corporation, AstraZeneca, and Genentech. B.K. has received honoraria from Boehringer-Ingelheim and Sanofi-Bristol Myers Squibb. D.K. has received honoraria from Boehringer-Ingelheim. The remaining authors have no disclosures.

Received May 13, 2007. Accepted in final form May 23, 2008.

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Spontaneous subcutaneous tissue haematoma associated with warfarin

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Spontaneous subcutaneous tissue haematoma associated with warfarin

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1. Nuno Cercas Pinheiro1,
2. Ana Lopes1,
3. Ana Camões2,
4. Micaela Seemann Monteiro2

1. ¹Department of Medicine I, Hospital Egas Moniz, CHLO, Lisbon, Portugal
2. ²Emergency Department H. São Francisco Xavier, CHLO, Lisbon, Portugal

1. Correspondence to
   Dr Nuno Cercas Pinheiro, ncercaspinheiro{at}gmail.com

http://dx.doi.org/10.1136/bcr-2016-215134

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Description

A 75-year-old man with a history of non-valvular atrial fibrillation anticoagulated on warfarin for the past 5 years without any prior complications presented to the emergency department with a cutaneous haemorrhagic lesion on his right lower limb, developed within the previous 24 h. There was no history of local skin lesion or trauma, and no infection or erroneous warfarin overdose.

Physical examination highlighted voluminous haematic phlyctena in the anterior, lateral surface of the right leg, surrounded by a large haematoma (figure 1A, B). Laboratory results revealed a supra therapeutic international normalised ratio (INR) (5.9), with no evidence of anaemia, nor of hepatic or renal abnormalities, and no signs of infection. A soft tissue ultrasound was performed revealing a large and heterogeneous haematoma of the local subcutaneous tissue, without muscular involvement, measuring 15×5 cm, compatible with the diagnosis of acute/subacute haematoma.

Figure 1

(A) Subcutaneous haematoma of the right leg with large haematic phlyctena; (B) detailed view of the lesion.

Drainage of the haematic phlyctena was then performed, as well as correction of INR with fitomenadione and human prothrombin complex. Self reabsorption of the haematoma was achieved in the following days, without further evidence of haemorrhagic complications. The patient was discharged on day 5 of admission and placed on dabigatran.

Despite decades of experience, warfarin still continues to be associated with haemorrhagic events.1–3 It is estimated that in 1 year, up to 6. 5% of patients on anticoagulant therapy will experience a major bleeding event affecting their soft tissue, gastrointestinal tract or urinary tract.3 Approximately 1% of patients will develop a fatal bleed, often an intracranial haemorrhage.3 As far as the authors are concerned, this is the first warfarin-related spontaneous subcutaneous tissue haematoma of the lower limb reported in the literature. Clinicians should be aware of sporadic fluctuations of INR, even if the warfarin scheme is accomplished and regular INR control performed. Large haematomas such as that being reported can be life threatening, thus correction of the underlying coagulation abnormalities and close monitoring of the patient should be assured.1–3

Learning points

• Despite prescription compliance and regular INR control, warfarin can be associated with spontaneous haemorrhagic events, even with moderately supratherapeutic INR.

• Correction of the coagulation disorder should be performed using fitomenadione, fresh frozen plasma or human prothrombin complex, with an individualised approach.

• Maintaining oral anticoagulation after a significant bleeding event is not consensual. However, novel oral anticoagulants could be a valid option after major bleeding, because of their shorter duration of action and new targeted antidotes.

Acknowledgments

The authors would like to thank Dr Joana Alvarenga, Dr João Pereira and Dr Alberto Mello e Silva, for their contribution to this article.

References

1. ↵
   1. Roca B,
   2. Roca M

   . The new oral anticoagulants: reasonable alternatives to warfarin. Cleve Clin J Med 2015;82:847–54. doi:10.3949/ccjm.82a.14052

2. ↵
   1. Tideman PA,
   2. Tirimacco R,
   3. St John A, et al

   . How to manage warfarin therapy. Aust Prescr 2015;38:44–8. doi:10.18773/austprescr.2015.016

3. ↵
   1. Zareh BS,
   2. Davis BS,
   3. Henderson MD

   . Reversal of warfarin-induced hemorrhage in the emergency department. West J Emerg 2011;12:386–92. doi:10.5811/westjem.2011.3.2051

View Abstract

Footnotes

• Contributors All authors contributed equally to management of the patient as well as writing the article.

• Competing interests None declared.

• Patient consent Obtained.

• Provenance and peer review Not commissioned; externally peer reviewed.

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Facelift (rhytidectomy, facelift, SMAS-lifting, SMAS-lifting) Overview

Facelift (rhytidectomy, facelift, SMAS-lifting, SMAS-lifting) is a cosmetic surgical procedure to create a younger looking face. The procedure can reduce sagging or wrinkling of the skin on the cheeks and chin, as well as other changes in the shape of your face (gravitational ptosis of the soft tissues of the face) that occur with age.

During a facelift (SMAS-lifting, SMAS-lifting), a flap of skin on each side is pulled back and the tissues under the skin are surgically reshaped to restore the contour of the face to a more youthful shape. Before the flap is sutured, excess skin is removed.

A neck lift (platysmaplasty, neck plastic) is often performed as part of a facelift to reduce fat deposits and sagging skin on the neck. To remove excess fatty tissue in the neck and chin area, direct fat excision or liposuction of the chin area or liposuction of the neck is used.

Facelift – Facelift will not reduce fine lines or deep wrinkles in the skin, nor will it reduce damage from sun exposure. Other cosmetic procedures may affect the appearance or quality of the skin itself.

Why is facelift performed – face and neck lift?

With age, the appearance and shape of the face change due to normal age-related changes. The skin becomes less elastic and looser, and fat deposits decrease in some areas of the face and increase in others. Age-related changes in the face that can be reduced with a facelift include the following:

* Sagging cheeks and neck

* Excess skin in the lower face and neck

* Deepening of the nasolabial and oral folds

* Sagging skin and excess fat in the cervical region (if the procedure includes a neck lift – platysmaplasty)

upper lip or uneven skin color.

Risks of facelift, facelift, facelift SMAS-lift, SMAS-lifting

Facelift surgery, especially SMAS-lifting, can cause complications. Some of them can be managed with appropriate care, medications, or surgical correction. Long-term or permanent complications, although rare, can cause significant changes in appearance. Risks of a facelift or facelift include:

* Facial hematoma. Accumulation of blood under the skin, causing swelling and pressure on surrounding tissues. Facial hematoma is the most common complication of facelift surgery – forehead plasty (endoscopic forehead and brow plasty). Bruising, which usually occurs within 24 hours of facelift surgery, is treated promptly with surgery to prevent damage to the skin and other tissues.

* Scar. Postoperative scars after facelift, facelift, facelift, SMAS-lifting, SMAS-lifting remain permanent, but are usually hidden behind the hairline and the natural contours of the face and ear. Rarely, incisions can result in raised red scars. Corticosteroid injections or other treatments may be used to improve the appearance of scars.

* Damage to the facial nerve. Nerve injury from a facelift or plastic surgery, although rare, can temporarily or permanently affect the nerves that control sensation or muscles. Temporary paralysis of individual muscles during a facelift resulting in an uneven appearance or facial expression, or temporary loss of sensation, can last from a few months to a year. Surgical interventions may offer some improvement.

* Hair loss after facelift or SMAS lifting. The patient may experience temporary or permanent hair loss near the incision sites. Permanent hair loss can be solved with hair follicle skin grafting surgery.

* Loss of skin due to necrosis after a facelift or SMAS lift. Rarely enough, a facelift – SMAS-lifting can disrupt the blood supply to the soft tissues of the face. However, if this happens it can lead to skin loss. Damage to the surface layer of the skin is treated with medications, appropriate wound care, and, if necessary, a procedure to minimize scarring.

Like any other major surgery, the facelift, the SMAS lift presents a risk of bleeding, infection, and an adverse reaction to anesthesia. Certain medical conditions or lifestyle can also increase the risk of complications. Some factors may pose a significant risk or lead to adverse outcomes, and your physician may advise you to refrain from a facelift, facelift, or SMAS lift.

* Risks include medicines or dietary supplements that thin the blood. Blood-thinning medications or supplements can affect blood clotting and increase the risk of bruising after surgery. These drugs include blood thinners (Coumadin, Plavix, others), aspirin, non-steroidal anti-inflammatory drugs (NSAIDs), ginseng, ginkgo biloba, fish oil, and others.

* Medical causes of complications in facelift, SMAS-lifting. If you have a disease that prevents blood clotting, you will not be able to do a facelift, SMAS-lift. Other conditions, such as poorly controlled diabetes or high blood pressure, increase the risk of poor wound healing, bruising, and heart complications and facelifts.

* Smoking. Smoking significantly increases the risk of poor wound healing, bruising, and skin loss after a facelift – SMAS.

* Weight fluctuations. If you have a history of gaining and losing weight repeatedly – factors that affect the shape of your face and the condition of your skin – the result of facelift surgery – facelift may be unsatisfactory or satisfactory only for a short time.

How is the preparation for facelift surgery – SMAS lifting, facelift.

First, there is a conversation with a plastic surgeon about a facelift, facelift or SMAS lift. The specialist collects the history and makes a preparation plan for the facelift.

* Case history and examination. Prepare to answer questions about past and current health conditions, previous surgeries, previous plastic surgeries, complications from previous surgeries, history of smoking, drug or alcohol use. Your surgeon will perform a physical examination, may ask your doctor for recent records, or book a consultation with a specialist if there is any concern about your ability to undergo facelift surgery.

* Medication review. List the name and dosage of any medications you take regularly, including prescription drugs, over-the-counter drugs, herbals, vitamins, and other supplements.

* Examination of facial features. Your plastic surgeon will take pictures of your face from different angles and close up some of the features. The surgeon will also examine bone structure, face shape, fat distribution, and skin quality to determine your best facelift options.

* Expectations. Your surgeon will ask questions about your expectations for the results of a facelift. It will help you understand how a facelift, SMAS lifting, will change your appearance, and what it cannot change, for example, fine wrinkles or natural asymmetries on your face.

Before facelift, facelift, SMAS:

* Follow medication directions. You will receive instructions on which medicines to stop taking and when. For example, you will likely be asked not to stop taking any medication that lowers or supplements blood pressure for at least two weeks prior to surgery. Talk to your healthcare provider about which medications are safe to take or if your dosage needs to be adjusted.

* Face, body and hair are washed before facelift surgery. You will most likely be asked to wash your hair and face with a germicidal soap the morning before your facial lift surgery.

* Starvation or cessation of food intake 4-6-8 hours before face plastic surgery, facelift. Or you will be asked not to eat anything after midnight before a facelift. You will be able to drink water and take medication approved by your surgeon.

* Help during convalescence. If your facelift is being done on an outpatient basis, schedule someone to drive you home after surgery and stay with you the first night after surgery.

What to expect

A facelift (facelift, CMAS) can be done in a hospital or outpatient surgical facility.

Before the start of the facelift procedure

Sometimes the procedure is carried out with sedation and local anesthesia, which numbs the area of ​​the operation. In other cases of SMAS lifting, general anesthesia is recommended, during which the patient is in a state of sleep of varying degrees of depth.

During a facelift or SMAS facelift

In general, a facelift includes skin tightening and tightening of deep facial structures and muscles. Fat on the face and neck can be redistributed, removed or introduced additionally into separate areas – face lipofilling. The skin of the face is then reattached to the newly positioned contours of the face, the excess skin is removed, and the wound is sutured or taped.

The incisions for the procedure depend on the methods to be used and the preference of the patient. Options include:

* Traditional facelift – classic SMAS-lifting (SMAS-lifting) starts in the temporal region, continues down and around the front of the auricle and ends behind the ears in the occipital region. A separate small incision can be made under the chin to improve the appearance of the neck, the so-called. platysmaplasty.

* A limited incision is a shorter incision that starts at the hairline just above the ear, wraps around the front of the ear, but does not extend all the way down to the bottom of the head.

* The neck lift incision starts in front of the earlobe and continues around the ear at the bottom of the head. A small incision is also made under the chin – a platysmaplasty.

Facelift-facelift usually takes two to four hours, but may take longer if other cosmetic procedures are performed at the same time, such as eyelid surgery, forehead plastic surgery, platysmaplasty, facial lipofilling, laser skin resurfacing, and other procedures.

After facial lift, SMAS lift

After a facelift, you may experience:

* Mild or moderate pain

* Drainage behind the ear

* Swelling in the area of ​​the operation and even in distant areas of the face

* Bruising or redness in the area of ​​the facelift operation

90 003* Numbness in the cheeks or eyelids

Contact your doctor immediately after your facelift if:

* Severe pain on one side of your face or neck within 24 hours of your surgery.

* Difficulty breathing

* Chest pain

* Irregular heartbeat

The surgery area after a facelift will most likely be covered with bandages that provide light pressure to minimize swelling and bruising. Through the drains within 1-2 days, blood or liquid may separate.

In the first few days after facelift (SMAS) surgery:

* Rest with your head up

* Take painkillers as recommended by your doctor

* Apply cool packs to your face to relieve pain and reduce swelling

Follow-up appointments after a facelift

You will have several follow-up appointments for the next two months after your surgery. These will include the following:

* The day after surgery, your surgeon will likely remove your drainage tube, apply antimicrobial ointment to your incisions, and apply new bandages to your face.

* Two to three days after a facelift, you can switch from wearing a bandage to wearing an elastic face mask.

* About a week after your surgery, your doctor will remove your stitches and evaluate your wound.

* Follow-up visits are likely to be scheduled to monitor your recovery.

Self-Care at Home

Self-care at home for the first three weeks will help you recover and minimize the risk of complications:

* Follow wound care instructions as directed by your surgeon.

* Twice a day, treat postoperative sutures with an antiseptic solution or betadine.

* Follow instructions on when you can start using shampoo and soap and which types can be used.

* Wear clothes that fasten at the front (not clothes that pull over your head).

* Avoid excessive pressure or movement in and around incisions.

* Avoid using makeup.

* Avoid vigorous or aerobic activities or sports.

* Avoid direct sun exposure to the incision for three weeks and use sunscreen with SPF 30 or higher.

* Avoid dyeing, bleaching or perming your hair for at least six weeks.

A few weeks after your facelift, you can style your hair to hide the remaining traces of the operation. You can also postpone attending large social events for a couple of months, when you are likely to feel at ease again.

Results

Facelift – facelift, SMAS facelift can give the face and neck a more youthful appearance. The results of a facelift are not permanent. With age, facial skin may continue to undergo age-related changes, but with the correct and radical approach to performing facelift surgery, manifestations of gravitational ptosis will be minimal. In general, facelift – facelift can be effective for life.

Hematoma: types, symptoms, images, causes and treatments

• What is a hematoma?
• What are the causes of hematoma?
• What are the symptoms and signs of a hematoma?
• When should I seek medical attention for a hematoma?
• How is a hematoma diagnosed?
• How to treat a hematoma?
• Can I treat a hematoma myself?
• How to treat a hematoma?
• Should I consult a doctor?
• Can a hematoma be prevented?
• What are the prospects after a hematoma?

What is a hematoma?

A hematoma is usually defined as an accumulation of blood outside of blood vessels. Most often, hematomas are caused by damage to the wall of a blood vessel, causing blood to leak from the blood vessel into the surrounding tissues. A hematoma can result from damage to any type of blood vessel (artery, vein, or small capillary). Hematoma usually describes bleeding that has more or less clotted, while hemorrhage means active, ongoing bleeding.

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Hematoma is a very common problem that many people experience at some point in their lives. Hematomas can be seen under the skin or nails as purple bruises of various sizes. Bruises on the skin can also be called bruises. Hematomas can also occur deep within the body where they may not be visible. Hematomas can sometimes form a mass or lump that can be felt. Sometimes hematomas are named based on their location. Here are some examples:

• Subdural hematoma: hematoma between brain tissue and the inner lining of the brain
• Spinal epidural hematoma: hematoma between the vertebrae of the spine and the outer shell spinal cord
• Intracranial epidural hematoma: hematoma between the skull and outer lining of the brain
• Subungual hematoma: Hematoma under the nail
• Intra-abdominal, peritoneal or retroperitoneal hematoma: intra-abdominal hematoma
• Ear or ear hematoma: hematoma between ear cartilage and overlying skin
• Spleen hematoma: hematoma in the spleen
• Liver hematoma: hematoma in the liver

Most hematomas resolve spontaneously over time as residual blood is removed and the blood vessel wall is repaired by the body’s repair mechanisms. In other cases, surgical removal or evacuation of blood from the hematoma becomes necessary depending on its symptoms or location.

What are the causes of hematoma?

The most common cause of hematoma is injury or trauma to the blood vessels. This can occur as a result of any damage to the blood vessels that can compromise the integrity of the blood vessel wall. Even minimal damage to a small blood vessel can lead to a hematoma. For example, a hematoma under the nail (subungual hematoma) may result from a minor injury to the nail or a light blow to an object.

More serious injuries may cause larger bruises. A fall from a height or being in a car accident can cause noticeable heavy bleeding under the skin or inside body cavities (chest or abdomen).

Other types of tissue damage that cause hematomas can result from any type of surgery, invasive medical or dental procedures (eg, biopsy, incision and drainage, cardiac catheterization), and drug injections (eg, insulin, anticoagulants, vaccines). . Because these procedures damage nearby tissues and blood vessels, bruising can often form around the procedure site.

Occasionally, a hematoma may occur spontaneously without any identifiable cause or memory of any particular trauma or injury.

Some blood thinners may increase the risk of hematoma formation. People taking medications such as Coumadin (warfarin), Plavix (clopidogrel), aspirin, Persanthin (dipyridamole)) or aspirin-containing products (eg Alka Seltzer) may develop a hematoma much more easily and with less severe blood vessel damage than other people . These drugs impair the blood’s ability to clot, and therefore a small injury to the blood vessel becomes more difficult to repair, resulting in a hematoma.

Other common medications and supplements that may increase the tendency to bleed include:

• vitamin E,
• non-steroidal anti-inflammatory drugs or NSAIDs such as ibuprofen (Motrin, Advil, Alev),
• garlic supplements, and
• Ginkgo biloba .

Thus, the list of drugs that cause excessive bleeding includes:

• warfarin (Coumadin),
• clopidogrel (Plavix),
• aspirin,
• aspirin products (Alka Seltzer),
• dipyridamole (persanthin),
• vitamin E,
• NSAIDs, e.g. ibuprofen, motrin, advil, aleve,

90 172 garlic supplements and

• Ginkgo biloba.

There are also certain medical conditions that may pose an additional risk of bruising. Individuals with the following conditions are potentially at higher risk of hematomas:

• chronic (long-term) liver disease,
• excessive alcohol consumption,
• bleeding disorders (eg, hemophilia and von Willebrand disease),
• blood cancer, or
• low platelet count (thrombocytopenia).

What are the symptoms and signs of a hematoma?

The symptoms of a hematoma usually depend on its size and location. Pain, swelling, redness, and bruising are common symptoms of a hematoma in general. Some symptoms characteristic of the localization of the hematoma:

• Symptoms of subdural hematoma : headache, neurological problems (weakness on one side, difficulty speaking, falling), confusion, convulsions.
• Epidural hematoma symptoms: back pain, weakness, loss of bowel or bladder control
• Subungual hematoma symptoms: nail pain, nail weakness, nail loss, nail disfigurement s spleen, liver or peritoneum: abdominal pain, side pain

Sometimes even very large hematomas do not have any symptoms. For example, if the bleeding occurs inside the abdomen, it may increase to a very large size before causing any symptoms. This can happen because the hematoma can spread in a relatively free space without pressing on any organs to cause pain or other symptoms.

On the other hand, a small bruise under the nail can cause severe pain because the blood expands into a very narrow space under the nail bed and causes inflammation and irritation of the nearby nail and skin, resulting in pain and swelling.

Depending on the location of the hematoma, a mass or lump can sometimes be felt.

When should I seek medical attention for a hematoma?

A hematoma can be treated by a doctor if symptoms are severe or continue to increase in size. For example, a hematoma in the brain (subdural) or an epidural hematoma usually requires immediate medical and surgical attention, especially if they are associated with neurological problems.

Physicians who routinely care for patients with hematoma are emergency room physicians, emergency physicians, surgeons, neurosurgeons, and internal medicine physicians.

How is a hematoma diagnosed?

Examination of a hematoma includes a physical examination and a detailed medical history. There are usually no specific blood tests to evaluate for a hematoma. However, depending on the situation, tests including a complete blood count (CBC), coagulation panel, chemistry and metabolic panel, and liver tests may be useful in evaluating a person with a hematoma, as well as assessing any underlying conditions and evaluating whether whether they are responsible for the formation of a hematoma.

Imaging studies are often needed to diagnose hematomas within the body.

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• Computed tomography (CT) of the head can reliably diagnose subdural hematoma.
• Abdominal CT is a good test for suspected hematoma in the abdominal cavity (intra-abdominal, hepatic, splenic, retroperitoneal, abdominal).
• Magnetic resonance imaging (MRI) is more reliable than computed tomography in detecting epidural hematomas.

How to treat a hematoma?

Treatment of hematoma depends on location, symptoms and clinical situation. Some may not need treatment at all, while others may be a medical emergency.

Can I treat a hematoma myself?

Superficial (subcutaneous) hematomas can be treated with simple home treatments. Most injuries and bruising can be treated with rest, icing, compression, and elevation of the area. This is remembered by the abbreviation FIG . These measures usually help reduce inflammation and reduce its symptoms.

• p is
• i ce (apply ice or cold compress for 20 minutes, 4-8 times a day.)
• C ompress bandages.)
• IS levate (It is recommended to raise the injured area above the level of the heart.)

If using ice packs, apply an ice pack or cold pack for 20 minutes 4 to 8 times a day. Compression can be achieved with elastic bandages, it is recommended to raise the injured area above the level of the heart.

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How to treat a hematoma?

Some small and asymptomatic bruises do not require any medical treatment. On the other hand, symptomatic or localized hematomas sometimes require medical or surgical treatment.

Although there is no specific medication for the treatment of hematomas, treatment of any associated symptoms can be achieved with medication. For example, pain from a hematoma can be treated with painkillers such as acetaminophen (Tylenol).

Surgical drainage is a common treatment for some hematomas. The presence of symptoms and the location of the hematoma usually determine what type of procedure is needed and how urgently it needs to be done. For example, a subdural hematoma that presents with symptoms such as headache, weakness, or confusion may require urgent drainage by a neurosurgeon. Conversely, if a subdural hematoma is considered asymptomatic and chronic, it can be left alone and occasionally monitored with imaging studies (computed tomography).

In addition, a subungual hematoma with severe discomfort can be expelled through the nail to allow blood to drain from the space between the nail and the underlying tissue. Large subungual hematomas that remain in place can sometimes damage the nail and cause it to die and fall out. Removal of such hematomas can save the overlying nail.

If there is any underlying cause or contributing factor that predisposes to bleeding, its correction or treatment may also be a necessary step in the management of hematomas. For example, if a person with a hematoma is taking a blood-thinning medication for another condition, the attending physician may stop taking or even stop taking the blood-thinning medication, depending on the individual situation.

Should I consult a doctor?

The location, symptoms, and size of the hematoma are typical factors in determining appropriate follow-up. For example, a symptomless (asymptomatic) small subdural hematoma may only require a repeat head CT scan every few months for follow-up. On the other hand, a large leg hematoma that has been opened and drained may be observed for several days to ensure the expected improvement.

Can a hematoma be prevented?

It is not entirely possible to prevent all hematomas. However, the prevention of hematomas in certain situations deserves special attention.

In people, especially older people, who take blood thinners or antiplatelet drugs (aspirin or clopidogrel), falls are a common cause of injury and bruising.