Professional Documents
Culture Documents
Auteurs :
Dr Dabreteau Aurélie
Dr Mallet Vincent
Dr Allo Jean-Christophe
1) Messages importants :
Evolution ultime de toutes les maladies chroniques du foie, la cirrhose est un état précancéreux.
La cirrhose est soit compensée, c’est à dire asymptomatique, soit décompensée : des signes d’insuffisance
hépatocellulaire sont alors présents. Une cirrhose compensée est évoqué si le foie est ferme à la palpation ou
dysmorphique à l’imagerie dans un contexte évocateur. Toute cirrhose, même compensée, peut se compliquer
d’une hypertension portale ‘occulte’. La splénomégalie associée à ma cirrhose est le reflet de l’hypertension
portale.
Tous les patients ayant une cirrhose grave ont une diminution du débit de filtration et sont à risque d’aggraver
brutalement leur fonction rénale, notamment après injection de produits néphrotoxiques (iode, aminosides,
AINS).
Tout patient cirrhotique décompensé est infecté ou va s’infecter. Toute cirrhose décompensée est en train de
saigner ou va saigner.
La plupart des cirrhotiques graves suivis sont traités par bêtabloquants non-cardiosélectifs.
Une fois le diagnostic établit, surtout si patient suivi en hépatologie à Cochin, prévenir les médecins du
service du Pr Pol. Poste 13003, 13007. Demander le chef de la salle, responsable des avis et des admissions
dans le service.
2) Physiopathologie :
L’insuffisance hépatocellulaire est une inadéquation entre besoins de l’organisme (synthèse, détoxication) et
réserve fonctionnelle hépatique. Les signes d’insuffisance hépatocellulaire (> 5 angiomes stellaires dans le
territoire cave supérieur, ictère, encéphalopathie, hypogonadisme, hypocoagulabilité, hypercinésie circulatoire,
ongles blancs, érythrose palmaire, oedèmes des membres inférieurs, propension aux infections…)
L’hypertension portale est secondaire à une élévation des résistances intrahépatiques. L’élévation de la
pression portale est responsable de l’ouverture de shunts préexistants entre le territoire porte et le territoire cave.
Les anastomoses porto-caves supérieures sont gastriques et oesophagiennes. La tension superficielle des
varices œsophagiennes (VO) dépend de la pression et du débit portal. Une majoration de la tension superficielle
des VO sous-muqueuses conduit à une rupture de leur paroi dénuée d’adventice. Toute pathologie responsable
d’une élévation du débit cardiaque (sepsis) ou de la pression portale (thrombose porte, souvent tumorale) peut
conduire à une rupture de VO. Les autres anastomoses porto-caves sont antérieures (circulation veineuse
collatérale abdominale), inférieures (varices rectales), postérieures (anastomoses spléno-rénales).
Une élévation du débit des shunts porto-caves peut conduire à une encéphalopathie (encéphalopathie porto-
cave) par défaut d’épuration du sang portal.
4) Tri IAO
Niveau 1 : DECHOCAGE
Niveaux 2 et 3 : BOX D’EXAMEN
Ascite
Régime :
Mesures associées :
O2 en fonction de la saturation
Surveiller :
hémodynamique, conscience, diurèse,
HGT.
ECG, RP
Pas de prise en charge spécifique Peut s’observer au cours de toutes hypertension portale, en
O2 en fonction de la saturation générale cirrhotique. Résulte de l’ouverture de shunts
artérioveineux pulmonaires, notamment au niveau des bases
des poumons.
5) Unité d’observation/USR
6) Orientation
De ce fait, l’argument formel du diagnostic positif est la mise en évidence de liquide par la ponction de la cavité
abdominale, généralement réalisée simplement au lit du malade lorsque l’ascite est en quantité importante.
Toutefois, les examens d’imagerie non-invasive sont très performants pour mettre en évidence cet épanchement
: échographie abdominale, tomodensitométrie ou IRM. Ils permettent de reconnaître les épanchements d’un
volume indétectable par l’examen clinique, limités aux poches et récessus péritonéaux (cul-de-sac de Douglas,
espace inter-hépatorénal), surtout quand ils sont inaccessibles à la ponction au lit du malade sans guidage
radiologique.
– chez un sujet atteint d’une maladie connue pour causer une ascite (voir plus bas au diagnostic
étiologique) ;
– une augmentation de volume de l’abdomen ;
– avec une matité abdominale déclive, mobilisable, à limite supérieure horizontale dessinant une courbe
concave en haut (anatomiquement) sur le sujet en décubitus dorsal.
La ponction abdominale pour mettre en évidence une ascite doit se faire selon les règles suivantes (fig.
32.1) :
– après avoir expliqué au patient la procédure, ce que l’on en attend, et ses désagréments ;
– après avoir vérifié que la rate n’occupe pas la fosse iliaque gauche, par la palpation ou la revue des
examens d’imagerie disponibles ;
– en un point situé à la jonction du tiers externe et du tiers moyen de la ligne joignant l’épine iliaque
antéro-supérieure gauche et l’ombilic, et en pleine matité ;
– après nettoyage et désinfection de la peau sur une large surface, en respectant les précautions
universelles et les règles de l’asepsie ;
– au moyen d’une aiguille ou d’un petit cathéter monté sur un mandrin, branchés sur une seringue
permettant de maintenir une légère aspiration ;
– en traversant rapidement la peau et la première épaisseur du pannicule sous cutané puis, plus
lentement, jusqu’à irruption du liquide dans le corps de la seringue, sans excéder un trajet d’environ 5
cm ;
– en faisant effectuer sur des échantillons du liquide prélevé des analyses cytologiques, microbiologiques,
et biochimiques appropriées.
Fig. 32.1. Repères du site de ponction d’ascite chez le sujet en décubitus dorsal
En pleine matité, à la jonction du tiers externe et du tiers moyen de la ligne joignant épine iliaque antéro-
supérieure et ombilic.
Une anesthésie locale peut-être utile chez les patients redoutant le geste.
Treatment Uses – For treatment of edema, including edema associated with heart failure or renal failure. As an
adjunct (for use with other medications) for treatment of acute volume overload states associated with heart
failure. For treatment of hypertension; most often employed in combination with other antihypertensive agents,
although probably effective if used alone. For treatment of ascites in patients with cirrhosis.
Furosemide is also used to improve pulmonary function in infants with bronchopulmonary dysplasia (BPD).
Nebulized furosemide may be beneficial for treatment of asthma in adults and children although the evidence
supporting this use is not overwhelming. Likewise, nasally inhaled furosemide has been used for treatment of
sinus congestion and for prevention of recurrent nasal polyps. There is also limited data suggesting that
nebulized furosemide may provide symptomatic relief of acute shortness of breath in patients with terminal
cancer. A small study of elderly men with nocturnal polyuria (frequent nighttime urination) given furosemide
six hours before bedtime demonstrated significant reduction in nighttime urination.
Furosemide belongs to a family of drugs called loop diuretics. The differences between loop and thiazide
diuretics result from where they act on the kidneys. Loop diuretics work by inhibiting sodium reabsorption from
the Loop of Henle (a more significant sodium reabsorption site) while thiazides inhibit reabsorption of sodium
in the early part of the kidney's distal tubules. Both cause increased excretion of sodium and water. The loop
diuretics produce a more aggressive and shorter lived diuresis; thiazides result in a gentler and more sustained
diuretic effect. Thiazides are more effective than loop diuretics for treating hypertension.
While furosemide is still the mainstay for treatment of acutely decompensated heart failure, it is slowly falling
out of favor for several reasons. The most important is that patients with heart failure are not uniformly volume
overloaded. In fact, 40 percent or more may be intravascularly volume depleted. Second, furosemide does not
work as quickly as previously thought in very sick patients. Finally, studies comparing treatment of acutely
decompensated heart failure found shorter lengths of hospital stay and fewer deaths in patients not given
furosemide.
Dosing and Administration – Usual adult oral dosing ranges from 20 to 80 milligrams per day, titrated to
effect up to 600 milligrams (daily). Larger doses are divided into twice daily administration. Single doses are
best taken in the morning to avoid sleep disruption from frequent nighttime urination.Intravenous (IV) dosing
for edema in adults is 20 to 40 milligrams, administered slowly. IV doses can be increased by 20 milligrams or
the same dose can be repeated at two hour intervals until the desired response is achieved. The final individually
determined dose can then be given once or twice daily. In acute volume overload states, best practice dosing
(found in many heart failure protocols) is a single IV bolus of double the patient's usual daily (24 hour) dose. IV
maximums top off at 4,000 milligrams per day. Injection rates faster than 20 mg/min can cause hearing
impairment; current literature recommends against administered furosemide any more rapidly than 4 milligrams
per minute. One way to slowly deliver any medication is to inject the drug into a proximal IV tubing port and
allow the drip rate to slowly deliver the drug to the patient (typical IV tubing administration sets have a 10-20
milliliter fill volume).
It should be noted when attempting to induce diuresis with escalating doses of furosemide that each patient
whose kidneys are capable of responding have a threshold below which no diuretic action occurs and a
(somewhat higher) threshold above which no greater diuretic effect is seen. Because these thresholds vary from
patient to patient and time to time, dosing changes should reflect this understanding. Contemporary critical care
practice often utilizes continuous infusions of furosemide to induce, maintain and adjust diuretic response.
Dosing for children and infants is typically 1 milligram per kilogram per dose either orally, IV or IM. Dose
titration and repeat administrations is much the same as for adults except that no more than 6 milligrams per
kilogram per day should be given to a child.
IV furosemide administered orally has potency similar to oral tablets, hence it can be given orally,, in
beverages, through feeding tubes when an oral solution is not readily available. In patients without IV access,
IV doses can be given IM, but have slower absorption.
Although most drug references say that furosemide can be taken with food or milk, oral doses taken with meals
may result in reduced plasma drug levels. Whether this is clinically significant remains controversial. If nausea
occurs with oral furosemide, taking the drug with food should reduce or eliminate this unpleasant side effect. To
avoid nocturia (nighttime urination), furosemide should be taken early in the day, and preferably before
breakfast (for maximal drug levels).
While no dosing adjustments are recommended for patients with renal insufficiency, it may take considerably
higher than normal doses to induce diuresis in patients with renal dysfunction. Patients with liver dysfunction
require higher than usual doses of furosemide and also experience prolonged absorption of oral furosemide. If
emergency diuresis is needed in patients with liver dysfunction, IV furosemide is preferred. No dosing
adjustments are required in the geriatric population.
Overdoses of furosemide generally result in volume depletion, hypotension and electrolyte imbalances.
Treatment should be supportive. Hypotension will respond to fluids. There is no specific antidote for
furosemide overdoses. Hemodialysis is ineffective in removing furosemide from the body.
During several national shortages of furosemide in the past, many EMS systems substituted bumetanide
(Bumex), another loop diuretic, for IV furosemide. Forty milligrams of furosemide is approximately equal to
1 milligram of bumetanide.
The kidneys excrete about 60 to 90 percent of furosemide. Feces contain 7 to 9 percent of furosemide and an
additional 6 to 9 percent is eliminated in bile. Furosemide is not removed by hemodialysis.
During pregnancy, diuretic use is generally avoided due to risk of decreased placental perfusion. Furosemide
does cross the placenta; increased fetal urine production and fetal electrolyte disturbances have been reported.
Whether furosemide is excreted in breast milk is uncertain. The World Health Organization suggests women
taking furosemide avoid breastfeeding.
Depending on manufacturer, furosemide comes in 20, 40 and 80 milligram tablets. Colors, shapes and sizes
vary by manufacturer. Tablets expire five years and solutions expire 42 months from manufacture date.
Injection solutions of furosemide are manufactured in a 10 milligram per milliliter concentration with vials or
ampules containing 2, 4, 8 and 10 milliliters. Furosemide is extremely light sensitive (hence, packaging in
darkly colored vials, ampules,and bottles). Exposure to light may cause discoloration; do not use furosemide
solutions or tablets with a yellow color. Refrigeration may result in drug crystallization or precipitation.
Rewarming may be performed without affecting the drug's stability. Infusions solutions of furosemide mixed in
NS or D5W are stable for 24 hours at room temperature. Oral solutions of furosemide come in 10 milligrams
per milliliter orange flavor and 40 milligrams per 5 milliliter pineapple-peach flavor. Furosemide should be
stored at room temperature between 59 – 86 F.
Cautions and Warnings – Furosemide should not be given to patients allergic to drugs containing sulfa.
Important Side Effects and Interactions – Side effects of furosemide are mostly related to diuretic effects, the
most significant of which are hypotension and decreased blood potassium levels (hypokalemia). Patients should
be instructed to rise slowly from sitting or lying positions to minimize lightheadedness or dizziness associated
with diuretic effects. Blood pressure and electrolyte levels should be checked frequently. Potassium
supplementation may be necessary. For reasons poorly understood, furosemide also has a tendency to increase
blood glucose levels in patients with diabetes. Nausea occurs occasionally with oral furosemide and can usually
be reduced or eliminated by taking the drug with food.
Incredibly for such a frequently used drug, there are virtually no published frequencies of side effects. Cases of
reversible and permanent hearing loss (ototoxicity) have been reported with furosemide. These have usually
been associated with rapid injection, administration to patients with renal failure, doses exceeding several times
the recommended maximums or administration with other ototoxic drugs.
There are 190 drugs are reported to interact with furosemide. Few of these could not be surmised from the
therapeutic actions of furosemide. Furosemide may increase the ototoxic effects of aminoglycoside antibiotics
and high dose salicylates. It may potentiate the action of succinycholine. There is a high risk of lithium toxicity
from reduced clearance of lithium when taken with furosemide. There may be a tendency towards worsening of
chronic renal insufficiency when furosemide is used in conjunction with NSAIDs.