Presentación de un caso clinico no común, fisuras costales por presión torácica negativa durante una apnea prolongada.

1. 1
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Dr.
Josep
Morera
29
noviembre
2016

2. 2
UN
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EN
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3. 3
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GUIÓN
1.-­‐
Introducción
2.-­‐
Presentación
de
Caso
Clínico
3.-­‐
Opinión
de
los
Asistentes
4.-­‐
DiagnósQco
5.-­‐
RaQonale
y
Discusión
6.-­‐
Conclusiones

4. 4
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NEJM
26
Oct.
1923

5. 5
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6. 6
UN
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UNA
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NO
DESCRITA
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7. 7
UN
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8. 8
Presentación
del
Caso
Clínico
F.H.P.
(30-­‐10-­‐2012)
-­‐ Varón
de
67
años
-­‐ No
fumador
-­‐ Jubilado.
Trabajó
como
comercial
de
una
FARMA
de
veterinaria
-­‐ Sedentario
-­‐ HepaJJs
a
los
4
años
-­‐
Adenoidectomia
a
los
6
años
y
apendicetomía
a
los
22
años
-­‐
Antecedentes
de
algunos
análisis
con
hiperglicemia
sin
diagnósJco
definiJvo
de
diabetes
-­‐ Acudió
a
nuestra
consulta
de
neumología
porque
tres
días
antes,
mientras
dormía,
despertó
por
dolor
torácico
intenso
brusco,
en
hemitórax
I.
Fue
atendido
en
el
Servicio
de
Urgencias
del
Hospital
CIMA.
-­‐ En
Urgencias
las
constantes
fueron
normales,
la
RX
de
tórax
fue
normal,
el
ECG
fue
normal.
La
analíJca
que
incluyó
CPK
y
Troponina
fue
normal.
-­‐ Estuvo
en
observación
durante
unas
horas,
se
le
administró
tratamiento
analgésico.
-­‐
Vista
la
evolución
fue
dado
de
alta
con
el
diagnósJco
de
dolor
torácico
y
la
indicación
de
acudir
a
consultas
externas
de
neumología.
UN
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9. 9
Presentación
del
Caso
Clínico
UN
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EN
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10. 10
Presentación
del
Caso
Clínico
La
exploración
en
la
consulta
fue
relaQvamente
anodina:
-­‐
Altura
1.72m
-­‐
Peso
80
Kg
-­‐
IMC
28.39
(sobrepeso)
-­‐
Distribución
troncular
de
la
grasa
-­‐
Auscultación
respiratoria
y
cardíaca
normal
-­‐
Sat.
O2
de
97%.
Fr
cardíaca
72
-­‐
No
edemas
-­‐
Flacidez
palpebral
-­‐
No
adenopagas,
no
organomegálias.
-­‐
Presión
sobre
pared
costal
izquierda
dolorosa
UN
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11. 11
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DiagnósQco
diferencial
de
dolor
torácico:
Origen
cardio-­‐vascular:
Ángor/infarto
de
miocardio
Disección
de
aorta
Angina
de
Prinzmetal/
S.
de
Takotsubo
PericardiJs
Necrosis
de
grasa
pericárdica
Otros
Origen
respiratorio:
Neumonía/pleuriJs
aguda
Infarto
pulmonar
Neumotórax/NeumomediasJno
Neoplasia
pulmonar
Mesotelioma
/Tumor
de
Pancoast
Otros
Presentación
del
Caso
Clínico

12. 12
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DiagnósQco
diferencial
de
dolor
torácico:
Origen
pared
torácica:
Fractura
costal/fisura
costal
Metástasis
costal/tumores
primiJvos
Síndrome
de
Tietze
Enfermedad
de
Mondor
Roturas
fibrilares
musculares/hematoma
Herpes
Zoster
Otros
Origen
otras
localizaciones:
Meteorismo
abdominal
Enfermedad
de
Bornholm
Espasmo
esofágico/Boerhaave
Hernia
discal
dorsal
Otros
Presentación
del
Caso
Clínico

13. 13
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Opinión
de
los
Asistentes

14. 14
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Opinión
de
los
Asistentes

15. 15
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Opinión
de
los
Asistentes
1.-­‐
Cuál
cree
que
es
el
diagnósQco
más
probable?
2.-­‐
Qué
dos
exploraciones
pediría?

16. 16
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DiagnósQco

17. 17
UN
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DiagnósQco

18. 18
UN
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DE
SAOS

19. 19
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DiagnósQco
Fisuras/fracturas
costales
por
estrés
secundaria
a
esfuerzos
repeJdos
para“vencer
apnea”durante
la
noche
Síndrome
de
Apnea
ObstrucQva
de
grado
severo

20. 20
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RaQonale
y
Discusión
Pistas:
1.
Episodio
nocturno
2.
Descartados
angor
e
infarto,
pleuriJs
y
pericardiJs
3.
Dolor
a
la
presión
torácica
local
4.
Signo
del
párpado
flácido(floppy
eyelid)
5.
IMC
de
28.39
con
distribución
de
grasa
troncular
6.Conocimiento
del
mecanismo
de
presión
negaJva
intratorácica
en
apnea
prolongada

21. 21
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RaQonale
y
Discusión

22. 22
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RaQonale
y
Discusión

23. 23
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RaQonale
y
Discusión
(24) or other antihypertensive drugs (25).
These facts raise the hypothesis that OSAS, besides favoring
the presence of arterial hypertension, could be a contributing
factor to dissection in some patients through the mechanical
stress on the aorta wall caused by repeated episodes of apnea
and hypopnea. Inspiratory efforts against an occluded upper
airway determine progressively negative intrathoracic pressures,
which reach final mean peak values of approximately Ϫ60 cm
H2O (8, 26). These negative pressures are transmitted to all
intrathoracic structures and have been related to worsening of
left ventricle function (27) and gastroesophageal reflux (28). In
an animal model, Peters and colleagues (29, 30) observed an
increase in systolic and diastolic aortic diameters during obstruc-
tive apnea episodes. In parallel to this development of progres-
sively negative intrathoracic pressures, a marked increase in
sympathetic activity and blood pressure is produced during ap-
neas, which at the end of the obstructive event may double
the basal systolic values (9, 31, 32). Upper airway obstructive
episodes during sleep are known to be frequently asymptomatic
(2) and may have been evolving for years before being clinically
detected. Thus, it could be speculated that in our patients, the
sudden rises in the transmural pressure of the aortic wall, re-
cations secondary to OSAS per se, rises in transmural pr
during upper airway obstructive episodes may have a partic
adverse effect on the recently surgically repaired thoracic
Because the anesthetic and postoperative management of
patients with OSAS benefits from specific measures (44, 4
believe that the early detection of OSAS could contribute to
perioperative management of these patients.
Our results indicate the need to assess the presence of
toms suggestive of OSAS in patients with thoracic aorta d
tion. Given the relative absence of sleepiness detected an
lack of specificity of other symptoms such as snoring, we b
that their presence should be additionally studied by s
screening tests such as nocturnal pulsioxymetry or a limited
study and, when the patient is stable, with full polysomnog
In summary, in this study, a high mean AHI was fou
patients with thoracic aorta dissection. We speculate th
coexistence of OSAS may impose an additional risk of
dissection in predisposed patients or determine worse evo
because of the increase in aortic transmural pressure im
Because effective treatment for OSAS is available, we b
its diagnosis should be considered in the overall assessm
patients with aortic dissection.
(24) or other antihypertensive drugs (25).
These facts raise the hypothesis that OSAS, besides favoring
the presence of arterial hypertension, could be a contributing
factor to dissection in some patients through the mechanical
stress on the aorta wall caused by repeated episodes of apnea
and hypopnea. Inspiratory efforts against an occluded upper
airway determine progressively negative intrathoracic pressures,
which reach final mean peak values of approximately Ϫ60 cm
H2O (8, 26). These negative pressures are transmitted to all
intrathoracic structures and have been related to worsening of
left ventricle function (27) and gastroesophageal reflux (28). In
an animal model, Peters and colleagues (29, 30) observed an
increase in systolic and diastolic aortic diameters during obstruc-
tive apnea episodes. In parallel to this development of progres-
sively negative intrathoracic pressures, a marked increase in
sympathetic activity and blood pressure is produced during ap-
neas, which at the end of the obstructive event may double
the basal systolic values (9, 31, 32). Upper airway obstructive
episodes during sleep are known to be frequently asymptomatic
(2) and may have been evolving for years before being clinically
detected. Thus, it could be speculated that in our patients, the
sudden rises in the transmural pressure of the aortic wall, re-
cations secondary to OSAS per se, rises in transmural pr
during upper airway obstructive episodes may have a partic
adverse effect on the recently surgically repaired thoracic
Because the anesthetic and postoperative management of
patients with OSAS benefits from specific measures (44, 4
believe that the early detection of OSAS could contribute to
perioperative management of these patients.
Our results indicate the need to assess the presence of
toms suggestive of OSAS in patients with thoracic aorta d
tion. Given the relative absence of sleepiness detected an
lack of specificity of other symptoms such as snoring, we b
that their presence should be additionally studied by s
screening tests such as nocturnal pulsioxymetry or a limited
study and, when the patient is stable, with full polysomnog
In summary, in this study, a high mean AHI was fou
patients with thoracic aorta dissection. We speculate th
coexistence of OSAS may impose an additional risk of
dissection in predisposed patients or determine worse evo
because of the increase in aortic transmural pressure im
Because effective treatment for OSAS is available, we b
its diagnosis should be considered in the overall assessm
patients with aortic dissection.
(24) or other antihypertensive drugs (25).
These facts raise the hypothesis that OSAS, besides favoring
the presence of arterial hypertension, could be a contributing
factor to dissection in some patients through the mechanical
stress on the aorta wall caused by repeated episodes of apnea
and hypopnea. Inspiratory efforts against an occluded upper
airway determine progressively negative intrathoracic pressures,
which reach final mean peak values of approximately Ϫ60 cm
H2O (8, 26). These negative pressures are transmitted to all
intrathoracic structures and have been related to worsening of
left ventricle function (27) and gastroesophageal reflux (28). In
an animal model, Peters and colleagues (29, 30) observed an
increase in systolic and diastolic aortic diameters during obstruc-
tive apnea episodes. In parallel to this development of progres-
sively negative intrathoracic pressures, a marked increase in
sympathetic activity and blood pressure is produced during ap-
neas, which at the end of the obstructive event may double
the basal systolic values (9, 31, 32). Upper airway obstructive
episodes during sleep are known to be frequently asymptomatic
(2) and may have been evolving for years before being clinically
detected. Thus, it could be speculated that in our patients, the
sudden rises in the transmural pressure of the aortic wall, re-
cations secondary to OSAS per se, rises in transmural pr
during upper airway obstructive episodes may have a partic
adverse effect on the recently surgically repaired thoracic
Because the anesthetic and postoperative management of
patients with OSAS benefits from specific measures (44, 4
believe that the early detection of OSAS could contribute to
perioperative management of these patients.
Our results indicate the need to assess the presence of
toms suggestive of OSAS in patients with thoracic aorta d
tion. Given the relative absence of sleepiness detected an
lack of specificity of other symptoms such as snoring, we b
that their presence should be additionally studied by s
screening tests such as nocturnal pulsioxymetry or a limited
study and, when the patient is stable, with full polysomnog
In summary, in this study, a high mean AHI was fou
patients with thoracic aorta dissection. We speculate th
coexistence of OSAS may impose an additional risk of
dissection in predisposed patients or determine worse evo
because of the increase in aortic transmural pressure im
Because effective treatment for OSAS is available, we b
its diagnosis should be considered in the overall assessm
patients with aortic dissection.

24. 24
UN
GRITO
EN
LA
NOCHE:
UNA
COMPLICACIÓN
NO
DESCRITA
DE
SAOS
RaQonale
y
Discusión
(24) or other antihypertensive drugs (25).
These facts raise the hypothesis that OSAS, besides favoring
the presence of arterial hypertension, could be a contributing
factor to dissection in some patients through the mechanical
stress on the aorta wall caused by repeated episodes of apnea
and hypopnea. Inspiratory efforts against an occluded upper
airway determine progressively negative intrathoracic pressures,
which reach final mean peak values of approximately Ϫ60 cm
H2O (8, 26). These negative pressures are transmitted to all
intrathoracic structures and have been related to worsening of
left ventricle function (27) and gastroesophageal reflux (28). In
an animal model, Peters and colleagues (29, 30) observed an
increase in systolic and diastolic aortic diameters during obstruc-
tive apnea episodes. In parallel to this development of progres-
sively negative intrathoracic pressures, a marked increase in
sympathetic activity and blood pressure is produced during ap-
neas, which at the end of the obstructive event may double
the basal systolic values (9, 31, 32). Upper airway obstructive
episodes during sleep are known to be frequently asymptomatic
(2) and may have been evolving for years before being clinically
detected. Thus, it could be speculated that in our patients, the
sudden rises in the transmural pressure of the aortic wall, re-
cations secondary to OSAS per se, rises in transmural pr
during upper airway obstructive episodes may have a partic
adverse effect on the recently surgically repaired thoracic
Because the anesthetic and postoperative management of
patients with OSAS benefits from specific measures (44, 4
believe that the early detection of OSAS could contribute to
perioperative management of these patients.
Our results indicate the need to assess the presence of
toms suggestive of OSAS in patients with thoracic aorta d
tion. Given the relative absence of sleepiness detected an
lack of specificity of other symptoms such as snoring, we b
that their presence should be additionally studied by s
screening tests such as nocturnal pulsioxymetry or a limited
study and, when the patient is stable, with full polysomnog
In summary, in this study, a high mean AHI was fou
patients with thoracic aorta dissection. We speculate th
coexistence of OSAS may impose an additional risk of
dissection in predisposed patients or determine worse evo
because of the increase in aortic transmural pressure im
Because effective treatment for OSAS is available, we b
its diagnosis should be considered in the overall assessm
patients with aortic dissection.
(24) or other antihypertensive drugs (25).
These facts raise the hypothesis that OSAS, besides favoring
the presence of arterial hypertension, could be a contributing
factor to dissection in some patients through the mechanical
stress on the aorta wall caused by repeated episodes of apnea
and hypopnea. Inspiratory efforts against an occluded upper
airway determine progressively negative intrathoracic pressures,
which reach final mean peak values of approximately Ϫ60 cm
H2O (8, 26). These negative pressures are transmitted to all
intrathoracic structures and have been related to worsening of
left ventricle function (27) and gastroesophageal reflux (28). In
an animal model, Peters and colleagues (29, 30) observed an
increase in systolic and diastolic aortic diameters during obstruc-
tive apnea episodes. In parallel to this development of progres-
sively negative intrathoracic pressures, a marked increase in
sympathetic activity and blood pressure is produced during ap-
neas, which at the end of the obstructive event may double
the basal systolic values (9, 31, 32). Upper airway obstructive
episodes during sleep are known to be frequently asymptomatic
(2) and may have been evolving for years before being clinically
detected. Thus, it could be speculated that in our patients, the
sudden rises in the transmural pressure of the aortic wall, re-
cations secondary to OSAS per se, rises in transmural pr
during upper airway obstructive episodes may have a partic
adverse effect on the recently surgically repaired thoracic
Because the anesthetic and postoperative management of
patients with OSAS benefits from specific measures (44, 4
believe that the early detection of OSAS could contribute to
perioperative management of these patients.
Our results indicate the need to assess the presence of
toms suggestive of OSAS in patients with thoracic aorta d
tion. Given the relative absence of sleepiness detected an
lack of specificity of other symptoms such as snoring, we b
that their presence should be additionally studied by s
screening tests such as nocturnal pulsioxymetry or a limited
study and, when the patient is stable, with full polysomnog
In summary, in this study, a high mean AHI was fou
patients with thoracic aorta dissection. We speculate th
coexistence of OSAS may impose an additional risk of
dissection in predisposed patients or determine worse evo
because of the increase in aortic transmural pressure im
Because effective treatment for OSAS is available, we b
its diagnosis should be considered in the overall assessm
patients with aortic dissection.
(24) or other antihypertensive drugs (25).
These facts raise the hypothesis that OSAS, besides favoring
the presence of arterial hypertension, could be a contributing
factor to dissection in some patients through the mechanical
stress on the aorta wall caused by repeated episodes of apnea
and hypopnea. Inspiratory efforts against an occluded upper
airway determine progressively negative intrathoracic pressures,
which reach final mean peak values of approximately Ϫ60 cm
H2O (8, 26). These negative pressures are transmitted to all
intrathoracic structures and have been related to worsening of
left ventricle function (27) and gastroesophageal reflux (28). In
an animal model, Peters and colleagues (29, 30) observed an
increase in systolic and diastolic aortic diameters during obstruc-
tive apnea episodes. In parallel to this development of progres-
sively negative intrathoracic pressures, a marked increase in
sympathetic activity and blood pressure is produced during ap-
neas, which at the end of the obstructive event may double
the basal systolic values (9, 31, 32). Upper airway obstructive
episodes during sleep are known to be frequently asymptomatic
(2) and may have been evolving for years before being clinically
detected. Thus, it could be speculated that in our patients, the
sudden rises in the transmural pressure of the aortic wall, re-
cations secondary to OSAS per se, rises in transmural pr
during upper airway obstructive episodes may have a partic
adverse effect on the recently surgically repaired thoracic
Because the anesthetic and postoperative management of
patients with OSAS benefits from specific measures (44, 4
believe that the early detection of OSAS could contribute to
perioperative management of these patients.
Our results indicate the need to assess the presence of
toms suggestive of OSAS in patients with thoracic aorta d
tion. Given the relative absence of sleepiness detected an
lack of specificity of other symptoms such as snoring, we b
that their presence should be additionally studied by s
screening tests such as nocturnal pulsioxymetry or a limited
study and, when the patient is stable, with full polysomnog
In summary, in this study, a high mean AHI was fou
patients with thoracic aorta dissection. We speculate th
coexistence of OSAS may impose an additional risk of
dissection in predisposed patients or determine worse evo
because of the increase in aortic transmural pressure im
Because effective treatment for OSAS is available, we b
its diagnosis should be considered in the overall assessm
patients with aortic dissection.
Otros
efectos
de
la
presión
negaQva
intratorácica:
1.-­‐
Reflujo
esofágico
2.-­‐
Hernia
de
hiato
3.-­‐
Tos
persistente
4.-­‐
Afectación
función
ventricular
izquierda/derecha
5.-­‐
Nicturia
6.-­‐
HTA
7.-­‐
Edema
pulmonar?

25. 25
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RaQonale
y
Discusión

26. 26
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RaQonale
y
Discusión

27. 27
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RaQonale
y
Discusión

28. 28
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RaQonale
y
Discusión

29. 29
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Conclusiones
1.-­‐
Los
cambios
de
presión
intratorácicos
en
el
SAOS
son
comunes
y
causan
diferentes
patologías
2.
La
repercusión
sobre
la
Aorta,
sobre
los
receptores
natriuréJcos
de
la
Aurícula
I
y
sobre
ambos
Ventrículos,
contribuye
a
patología
cardiovascular
secundaria
al
SAOS
3.-­‐
No
es
infrecuente
que
los
pacientes
con
SAOS
severo
se
quejen
de
dolores
torácicos
inespecíficos
4.-­‐
Se
ha
presentado
un
caso
no
descrito
de
fracturas
costales
producidas
por
Apneas
durante
el
sueño
(SAOS)

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