I have
the distinct advantage and pleasure of having an Internist as my spouse. Rarely a dinner goes by without a case
discussion. Recently, she brought up an
all-too-common case…
the distinct advantage and pleasure of having an Internist as my spouse. Rarely a dinner goes by without a case
discussion. Recently, she brought up an
all-too-common case…
One of
her ‘’favorite’’ ESRD patients had died suddenly at home after receiving his
in-center hemodialysis. The patient was
relatively young, notoriously non-compliant, had frequent fistula complications,
but no known cardiopulmonary disorders.
She asked, “what do you think did this?” “Could it have been a PE or something?”
her ‘’favorite’’ ESRD patients had died suddenly at home after receiving his
in-center hemodialysis. The patient was
relatively young, notoriously non-compliant, had frequent fistula complications,
but no known cardiopulmonary disorders.
She asked, “what do you think did this?” “Could it have been a PE or something?”
Depending
on your narrative, ESRD can be either a pro or anti-coagulant state. After all, they are exposed to heparin,
they’ve got uremic platelet dysfunction, etc.
However, multiple studies have revealed the incidence of PE is 7-fold
higher in ESRD compared to those with normal renal function (an incidence of PE
near that of patients with active malignancy). In fact, having a PE with
ESRD carries twice the mortality rate and hospitalization rate compared to
those with normal renal function. Post-mortem studies would argue pulmonary
embolism was a rare cause of death in ESRD, only 6.5% of hospital deaths in
ESRD patients were attributable to thromboembolism. Does this really make sense? Along with the
high chance of inherent bias in autopsy studies, the risk factors for thrombosis
in ESRD are seemingly endless; recent surgery, central catheterization, access thrombectomy,
hospitalization, proteinuria, immobility, inflammatory states, obesity, autoimmune
diseases and so on.
on your narrative, ESRD can be either a pro or anti-coagulant state. After all, they are exposed to heparin,
they’ve got uremic platelet dysfunction, etc.
However, multiple studies have revealed the incidence of PE is 7-fold
higher in ESRD compared to those with normal renal function (an incidence of PE
near that of patients with active malignancy). In fact, having a PE with
ESRD carries twice the mortality rate and hospitalization rate compared to
those with normal renal function. Post-mortem studies would argue pulmonary
embolism was a rare cause of death in ESRD, only 6.5% of hospital deaths in
ESRD patients were attributable to thromboembolism. Does this really make sense? Along with the
high chance of inherent bias in autopsy studies, the risk factors for thrombosis
in ESRD are seemingly endless; recent surgery, central catheterization, access thrombectomy,
hospitalization, proteinuria, immobility, inflammatory states, obesity, autoimmune
diseases and so on.
More
puzzling, is that recent studies have shown that pulmonary
hypertension (PH) in ESRD, so dubbed ‘Uremic Pulmonary Hypertension’ is a significant
entity. Some report a prevalence as
high as 50% by echocardiographic criteria, and around 10% by RHC when corrected for left sided heart failure, so called pre-capillary pulmonary hypertension. Currently the prevalence of chronic
thromboembolic pulmonary hypertension in ESRD is not known.
puzzling, is that recent studies have shown that pulmonary
hypertension (PH) in ESRD, so dubbed ‘Uremic Pulmonary Hypertension’ is a significant
entity. Some report a prevalence as
high as 50% by echocardiographic criteria, and around 10% by RHC when corrected for left sided heart failure, so called pre-capillary pulmonary hypertension. Currently the prevalence of chronic
thromboembolic pulmonary hypertension in ESRD is not known.
It would
follow that a pulmonary embolism on an already strained right ventricle would
seem a perfect storm for classic PE presentation. In fact, it has been previously postulated by
Kumar et al that increased co-morbidity burden, especially cardiovascular
complications associated with both these diagnoses, lead to diminished
cardiopulmonary reserve, increasing both severity of PE and associated
mortality. Yet, severe signs and
symptoms like hypoxia, chest pain, volume overload or persistent hypotension are
quite possibly overlooked, and sooner attributed to under or overaggressive
ultrafiltration, heart failure or coronary artery disease. There is a scarcity data on clinical
manifestations of PE in the ESRD population, predominantly case reports and
case series. Even DVT’s have been shown to present atypically with less extremity discomfort and far more upper
extremity DVT’s vs lower extremity (30% vs 10.8%).
follow that a pulmonary embolism on an already strained right ventricle would
seem a perfect storm for classic PE presentation. In fact, it has been previously postulated by
Kumar et al that increased co-morbidity burden, especially cardiovascular
complications associated with both these diagnoses, lead to diminished
cardiopulmonary reserve, increasing both severity of PE and associated
mortality. Yet, severe signs and
symptoms like hypoxia, chest pain, volume overload or persistent hypotension are
quite possibly overlooked, and sooner attributed to under or overaggressive
ultrafiltration, heart failure or coronary artery disease. There is a scarcity data on clinical
manifestations of PE in the ESRD population, predominantly case reports and
case series. Even DVT’s have been shown to present atypically with less extremity discomfort and far more upper
extremity DVT’s vs lower extremity (30% vs 10.8%).
Ok, but
wouldn’t sudden death point us in the right direction? The limited and outdated post-mortem data have
not supported massive PE as a common cause of sudden death, and a recent ERA-EDTA registry review suggest the proportion of deaths attributable to PE among
dialysis patients was only 0.7% over 2 years, barely above the general population,
at 0.5%. However, around 25% were either Sudden Death or Other, and as a
recent review by Makar and Pun pointed out the etiology of sudden death in ESRD
is quite commonly unknown and a significant number of cardiac arrests are not
shockable. One study in their review showing as many as 33%
of all sudden deaths in HD patients were non-ventricular arrhythmias including
asystole and pulseless electrical activity. Previous studies estimated that
massive pulmonary embolism accounts for up to 13% of unexplained cardiac
arrests, and the predominant rhythm of those arrests is pea or asystole in 95%
of cases. It begs, are we
missing VTE?
wouldn’t sudden death point us in the right direction? The limited and outdated post-mortem data have
not supported massive PE as a common cause of sudden death, and a recent ERA-EDTA registry review suggest the proportion of deaths attributable to PE among
dialysis patients was only 0.7% over 2 years, barely above the general population,
at 0.5%. However, around 25% were either Sudden Death or Other, and as a
recent review by Makar and Pun pointed out the etiology of sudden death in ESRD
is quite commonly unknown and a significant number of cardiac arrests are not
shockable. One study in their review showing as many as 33%
of all sudden deaths in HD patients were non-ventricular arrhythmias including
asystole and pulseless electrical activity. Previous studies estimated that
massive pulmonary embolism accounts for up to 13% of unexplained cardiac
arrests, and the predominant rhythm of those arrests is pea or asystole in 95%
of cases. It begs, are we
missing VTE?
It may be
justifiable to look for PE more often, and in fact all the registry data in the
world means little if we’re missing the diagnosis in the first place. It’s akin to dogs chasing cars, what would we
do if we caught one? Can we accept the risks of anticoagulation for sub-segmental
PE, or incidental PE? Would you feel safe using a NOAC? I suppose it depends on your narrative.
justifiable to look for PE more often, and in fact all the registry data in the
world means little if we’re missing the diagnosis in the first place. It’s akin to dogs chasing cars, what would we
do if we caught one? Can we accept the risks of anticoagulation for sub-segmental
PE, or incidental PE? Would you feel safe using a NOAC? I suppose it depends on your narrative.
Posted by Corey Cavanaugh DO
OGY-3 Internal Medicine Resident, University of Louisville
Yale Clinical Nephrology Fellow – July 2017
