The incarcerated umbilical hernia in a patient with the liver cirrhosis and ascites seems to be the rarest clinical entity. At any rate I have never seen it for 26 years of my practice at emergency surgery department. As a rule the hernial suc contains just a trifle of the ascite fluid, more seldom it may include an edge of the greater omentum. The small intestine is usually heavier than the fluid and sinks on the abdominal cavity bottom, whilst peritoneal adhesions occur in the ascites patient very rarely, I do not know why it goes this way. Far more frequent a case is the umbilical hernia suc skin necrosis with perforation.
However, the question you asked is of high practical importance without any doubt .
I dare to suggest for a case like this a sublay mesh repair with the abdominal cavity drainage point as far from the hernioplasty as possible. What of extreme significance is to avoid insertion of the drainage tube through the same wound lest it become infected and the plasty fail inevitably. One more thing, the procedure should be as mini-invasive and swift as only possible so that the anaesthesia duration can take shortest time (as commonly known, any sort of anaesthesia connects with hepatotoxicity and arterial hypotension that may lead by themselves the cirrhosis patient to tragical end).
So, if you do not mind, I have a question to you in my turn: what kind of anaesthesia would you prefer for such a patient?
I prefer for these patients a general anesthesia, mainly for surgical team convenience. Nevertheless, I agree with you that a general anesthesia comes with more hepatic toxicity. I have a very limited experience with umbilical hernia in cirrhotic patients. A far more experienced colleague, had recommended for this patient a local anesthesia with intravenous augmentation, by I had wanted a more extended dissection, a wider mesh and a more resistant reconstruction. I have finished by a tissue repair.
In conclusion, for my next case I will choose: a local anesthesia, a Rives-Stoppa repair, a Douglas pouch drain, and a closed suction retromuscular drain.
For cirrhotic patients without ascites fluid I would be much happier with a laparoscopic approach.
Thank you so much, for sharing me your experience!
Your 'next time' strategy is better choice for such a patient, I couldn't agree more.
Thank you for so high mark of my humble opinion! My experience based on 5 cases of the hernial suc perforation and the only incarceration (in patients with a cirrhotic ascites).
The optimal repair in this case is open mesh repair in sublay position (preperitoneal space); try not to open the hernia sac and you will not be in contact with the ascites fluid. Local anesthesia is favourable! no drain! single shot antibiosis! Good luck ;-)
Several questions to Dr.Bernhardt (to avoid a possible misunderstanding):
How do you imagine an incarcerated hernia surgery without opening of the sac?
Have you any experience of an intestine resection for strangulation under local anaesthesia? Actually, what kind of local anaesthesia did you mean? Spinal, epidural, or local one in a strict sense (nach Braun, infiltration)?
How do you suggest to suture or fix the mesh in place looking forward intraabdominal pressure to grow up due to undrained ascitis? Will it depends from a degree of the portal hypertension, or Child-Pew scale, or anything else?
There are too many questions, but I might be excused by the only hope to learn a little more about rare cases like these.
Thank you for your comments and questions. In case of irreponible hernia with incarcerated bowel we need to do an emergency operation with general anaesthesia. Preoperative contrast enhanced CT-scan shows you if you need to open the hernia sac or not. As you already mentioned in case of ascites a real incarceration is rather the exception than the rule.
In all other patients where a reposition of the hernia was succesful I recommend scheduled operation (means preoperative stabilisation of the patient --> treating hypoalbuminemia, thrombocytopenia, etc.) as mentioned before: local anaesthesia ("Strict sense"); I use a self expanding PTFE circle mesh with stripes; usually I dont fix the mesh (not necessary in the preperitoneal-sublay position); above the mesh I close the hernia ring (if possible - in small hernias) with non-absorbable sutures; of course the size of hernia is also essential; under 1cm I do not use meshes; above 8cm I do not use local anesthesia.
I hope you got the right answers. I am sorry that without explaining everything in detail some statements have been unclear...
Thank you for the most complete explanation! There is a profound strategy for ascitis patients elective hernia repair in your institution, so I shall take it, so to say, in my arsenal.
However, I dare to ask a couple of new questions more, if you please (not urgent!):
The topic is about incarcerated umbilical hernia management in the ascitis patient group. So my questions are devoted to this very group:
is it obligatory or not to drain the abdominal cavity in case of the real (small) intestine strangulation?
What CT data did (or would) you take into account that proved really that the loop was for sure alive or dead?
Actually, whether a surgeon ought to rely upon the CT data wholly and not to open the sac in case the haemorrhagic (and presumably infected) contents seen through its wall? In other words, what way would be the best choise to follow in questionable cases: to open the suc with risque to pollute the operational wound, or pose the hernia contents back into the abdominal cavity with its 'hernia water', as old authors called that fluid?
I must confess I have not found studies about the bacterial colonization degree of the hernial sac contents in incarceration in 'usual' patients, not to mention in the ascitis ones.
I understand your concerns; you are right as surgeons we should not rely soley to CT data; and indeed even without CT you will see based on the discomfort and pain after reposition of the hernia or after operation if the intestinal strangulation led to a dead bowel; in doubt I would risk a second look operation on demand (of course with opening the peritoneum) however so far all reponible hernias did not cause problems. In other cases where you need to widen the hernia ring, I also open the sac,in these cases you will find in a high number damage to the bowel.
The thing not to drain is that we experienced persisting fistula because of the ascites that were difficult to manage.
IMHO, 'the persisting fistula' can be managed in number of cases by a simple horseshoe-shaped suture closure, it is not the matter of concern when a surgeon deals with a life-threatening disease as incarcerated hernia at any rate.
Honestly to say, I prefer more aggressive (and archaic) strategy in doubtful situation restricted by the umbilical hernia patients, not multichambered hernia ones : the hernial sac should be opened and its contents revised. If the intestinal loop is alive, becoming rose and motile, the hernial fluid is presumably sterile or just little contaminated with bacteria, so that there is little concern of the future wound sepsis; alternatively, there is no choice except to open the sac and do what we have to do. I have a very experience to irrigate the incisional wound up by the water-soluble antiseptics as abundant as ever possible. This simple method saves the soft tissue from sepsis in almost all cases (with the only exception when the intestinal wall perforation has already occured and caused yet the immediate tissue necrosis).
Here is a review how to treat diuretic-resistant ascites which may (or might) be useful not for therapeutists only, but for some surgeons as well. It does really works!
There are some crucial questions in such cases: which organ exactly is incarcerated, and wheter the incarcerated content is vital or not, and is there an infection? So in my opinion laparoscopy is the most reliable option – you can reduce the hernia, can see what is incarcerated and wheter there are signs of necrosis, and also take fluid for culture. If there is a bowel necrosis the need of resection is clear. But if it is not the problem is always whether there is an infected ascites, as there is never been a good idea to place a mech in infected conditions. So better reduce the hernia, apply external pressure of the sac, for example with gauzes and fix them with adhesive bands or folio drape. Start antibiotics keeping the guidelines for the treatment of bacterial peritonitis in cirrhosis. Do not remove ascites if not visibly purulent, no drains, as they usually caused nearly uncontrollable homeostatic disturbances due to huge amount of fluid losed. When the patient is stable and infection is controlled by antibiotics you can move back to OR and do that what you prefer. I think the laparoscopic repair is better. So the philosophy is that there is absolutely no need to address both problems – incarceration and hernia itself in one stage in a patient that is usually not fit for surgery and had severe comorbidities. The exception might be the patients requiring bowel resection.
It comes from the currently evolving concept for the laparoscopic treatment of incarcerated inguinal hernia, surely common situation, and I just adapted slightly it to this so rarely seen scenario in cirrhotic pts with ascites. Just the mode of external compression is a maneuvre which comes from my practice in elective lap-repair of large-defect hernias, where I use it in order to prevent migration of the mesh within the fascial defect. I think still few centers experienced in laparoscopic hernia surgery used the mentioned strategy in incarceration now (personal communication), but the concept is relatively new, and I am not aware for published papers. I am also supporter of this approach, especially in elderly and severely comorbid population, but never had a case of patient with ascites and incarcerated umbilical hernia.
On the other hand this concept is older than hernia surgery – it is just laparoscopic reposition of the hernia, not manual. It is the same that we will do if manual reposition does not fail. So if someone agree manual reposition and interval operation why not to consider a little bit more invasive reposition :)
However, I dare to assume that there may be a difference between a common situation of incarcerated inguinal hernia and that one in cirrhotic and ascites patient in terms of better approach and way to reduce hernia, whenever possible. Furthermore, I dare to suppose that the more comorbidities, the higher portal pressure, and the more ascitis volume (etc.), the more invasive and traumatic will be laparoscopic approach and general anaesthesia.
I do know nothing about the interaction of the unevacuated (according to your advice) cirrhotic ascites and tension carboxyperitoneum and can hardly recommend to try this combination in practice.
The idea to "apply external pressure of the sac, for example with gauzes and fix them with adhesive bands or folio drape" does not seem reliable because 1) adhesive bands will hardly able to withstand the intraabdominal pressure except in the newborn child; 2) the ascites patients are rather inclined to exibit a skin irritation against longtime use of adhesive bands and stuff like these; 3) a 'good old' hernial bandage might be better for the case, but I would prefer the mesh being sutured to prevent its migration instead of its external compression. 4) usually the mesh will not become infective if it is connected nor with the skin, neither with the abdominal cavity, and was placed after careful lavage of the soft tissues incisional wound, even in case of 'frank' intestine necrosis.
At last, I cannot see why a surgeon should not use a limited ascites evacuation, for example, five liters volume was recommended in the article I mentioned above (see above for my hyperlink).
Thanks for your interesting point of view and comments. I will try to address all the points you questioned. My opinion is based on strong evidence whenever possible, and on experience of my clinic in HPB surgery when there is limited or no evidence. There is strong evidence that laparoscopic surgery is better tolerated even in cirrhotics with all the advantages of minimal invasion, and we never have doubt to prefer it in cirrhotics. And for external pressure you can choose whatever you think is useful, it is not so important. We are following the described way without any complication. There is also a widely accepted consensus not to use a mesh in contaminated and clean-contaminated conditions, I am just strongly following it. There is no lavage that can remove the infection, it only can reduce the number of bacteria and there is no discussion about that. It is safe to remove up to 3l of ascites or less only to reduce intraabdominal hypertension and its negative consequences on pulmonary function if present. The removal of ascites has his specific consequences in term on severe homeostatic disturbances, which can be lethal as we know from experience with cirrhotics. Do not forget that this is a surgical patient, not one with just refractory ascites. And the postoperative course in decompensated cirrhosis is unpredictable, but surely with higher morbidity and mortality compared to noncirrhotics. The literature is full of papers discussing the secure limit of ascites that can be removed in different conditions. We agree with authors accepting upper limit of 3l in one session in cirrhosis, and this is not absolute – actually we always carefully looking how that is tolerated. And finally it is not only safer, but cheaper – as the patient ultimately will continue to have ascitic loses, you will face with the fact how expensive is to treat all the disturbances (electrolytic imbalance, severe hypoalbuminemia etc.). So why just not try to prevent at least partially their aggravation (as they always are already present) – it is safer and cheaper. And the cirrhotics are surely specific population.
Thank you so much for this profound note , Dr.Alexander!
I would like to ask about peculiarities in the cirrhotic ascites patient laparoscopy. Are there any tricks you developed or pitfalls you discovered?
A propos 'there is no lavage that can remove the infection'... The sentence is not so simple as it looks like. As commonly known the bacteria count does really matter, and lavage diminishes it without any doubt.
Once upon a time one of my students asked me a 'childish' question: "There are microbes lurking everywhere, are't they? On the walls, on the floor, on various things surface. When anyone is walking or sitting, are he (or she) crashing them down?" :))
I think the meticulous preoperative preparation is the first key for any intervention in decompensated cirrhosis. Whenever possible the electrolytic imbalances, haemostatic and acid balance as well as hypoalbuminemia should be corrected preoperatively. The caloric intake and comorbidities should be carefully addressed. And if the patient had also diabetes or chronic renal failure it is very, very friable. Competent anesthesiologists deeply understanding the pathology of homeostasis in cirrhosis and ICU are invaluable. If possible use all the possibilities for diagnostic planning of your intervention, even you do not need them usually (i.e. abdominal CT in a cirrhotic preparing for hernia repair). The inflation pressure and other OR setup are the same as in noncirrhotics. Monitoring of exhaled CO2 is helpful, but if the operation is longer, you will realize that acidosis occurs by oozing which starts from the operative field (if you do more than simple umbilical hernia repair). So if you plan a complex intervention that will took more than 30-40 min take in consideration to exsuflate the abdomen from time to time for 2-3 min and ask the anesthesiologist to hyperventilate the patient. This helps in preventing hemostatic disturbances and aggravation of bleeding due to hypercapnic acidosis. The restricted i.v. infusion policy is also important.
Regarding your comments about infection I agree with you if we talk about noncirrhotics. Cirrhotics are immunocompromised population. They developed clinically significant sepsis in conditions where pts without cirrhosis had no problems. Classical examples are spontaneous bacterial peritonitis or hepatic failure & encephalopathy attacks caused by transient systemic/portal bacteremia which are frequent and had no consequences in healthy subjects. So we should be very careful with every detail.