**2. Assessing the patient**

We can think, out-of-the-book, abdominal emergencies as a devilish blend of dangerous ingredients. Diagnosing an acute abdomen is sorting out the different components from the mix to finally draw conclusions on its danger.

Ideally, we should be able to do it quickly, pragmatically, and in a costeffective manner.

We appreciate that there is a significant disparity in what can be used in different health systems. What is readily available in high-income countries, it is not (or is inexistent) in low-income countries. The authors' bias is to work in some of the best health systems in the world, at least according to the World Health Organization, where almost everything is available 24/7/365.

We all know the signs and symptoms of a patient with acute diverticulitis.

They usually have persistent moderate to severe abdominal pain with guarding and rebound tenderness located in the left lower quadrant or hypogastrium (Hinchey I–II), which turns to be diffused to all the abdominal cavity as the infection is no longer localized (Hinchey III–IV).

Nausea, vomiting, fever, and in some cases, dysuria can also be present in many patients.

In modern and mature health care systems, patients with diffuse peritonitis and septic shock should be diagnosed straightforwardly with a CT abdomen-pelvis with intravenous contrast. We never stress enough to our trainees, and during our M&M, how a speedy diagnosis contributes to saving lives. Also, we are very adamant that a CT without IV contrast is a suboptimal examination in almost all the emergency clinical situations. Acute kidney injury (AKI) or chronic renal failure (CRF) are not, and should not be a contraindication to obtain a good quality CT scan. The quantity of literature on the safety of modern IV contrasts is vast and easily searchable in PubMed.

CT scan gives us all the information we need; such as free fluid vs. localized collection, the distribution of free air, and direct signs of diverticulitis. Not infrequently,

**73**

hospitals.

*Damage Control in Hinchey III and IV Acute Diverticulitis*

be delivered within 1 h of the initial diagnosis of sepsis [7]:

1.Titrate oxygen to a saturation target of 94%.

3.Administer empiric intravenous antibiotics.

4.Measure serial serum lactates.

5.Start intravenous fluid resuscitation.

is as bad as all the others available [7–9].

2.Take blood cultures and consider source control.

6.Commence accurate urine output measurement.

Someone could argue that extremely sick patients, who are the ones who will require damage-control procedures, can be diagnosed on the spot by merely looking at them. They could also argue that a lot of scoring is useless and done only for scoring sake. We do not agree with them. It is imperative in our practice to assess the response to our treatment, and this can be done only if we have determined our starting point. We still use, as many other colleagues do, the concept and definitions of the "Surviving Sepsis Campaign: International Guidelines for the Management of Severe Sepsis and Septic Shock: 2012." We stress to our trainee the importance of assessing the patient and following their response to the treatment. Diagnosis at a glance also does not correlate with morbi-mortality, and it is not a common language used when dealing with other specialties, who would look upon your surgeon as a caveman. We use the Sepsis definition, and the p-POSSUM score as a minimum to assess patient severity and surgical risk. We appreciate that P-POSSUM has been criticized, and possibly is not the best scoring tool available. Let us say that p-POSSUM

Septic patients are treated according to the Surviving Sepsis Campaign Bundle. Upon arrival, once the acute abdomen has been identified (again, it is a clinical diagnosis!), blood cultures are taken, and broad-spectrum antibiotics are started along with intravenous fluid replacement. For each hour of delay of antibiotic

Which antibiotic should be administered is up to your hospital policies. Piperacillin/Tazobactam is the first choice in no-penicillin allergic patients in many

administration, there is a cumulative increase in mortality of 4%.

it informs us of other unknown conditions that could change the overall attitude such as multiple liver metastases, primary neoplasms of the large bowel or other

We agree that diagnosis is paramount, but treatment is our real goal. And treat-

An acute abdomen is a diagnosis based on clinical examination. Sepsis should be considered as the primary cause of an acute abdomen until proven otherwise. Sepsis can be identified within minutes by recognizing hypotension, tachycardia, tachypnea, and oliguria. Blood tests (White Blood Cells and C-Reactive Protein) together with venous or arterial blood gases (lactates) can add crucial information towards the final diagnosis of sepsis. Are they septic? Are they in septic shock? Usually, in acute diffuse peritonitis, from diverticulitis or other causes as well, the answer is many times, yes, they are already in septic shock. Some Health Systems, like the United Kingdom's National Health System (NHS), introduced the "Sepsis-Six." The Sepsis-Six consists of three diagnostic and three therapeutic steps—all to

*DOI: http://dx.doi.org/10.5772/intechopen.92669*

ment should start before diagnosis.

organs, etc.

*Damage Control in Hinchey III and IV Acute Diverticulitis DOI: http://dx.doi.org/10.5772/intechopen.92669*

*Trauma and Emergency Surgery - The Role of Damage Control Surgery*

status of the presenting patient [4].

number of surgeons, a safe option [1–6].

Damage Control Modality.

**2. Assessing the patient**

therapeutic strategy.

effective manner.

The clinical and surgical approach to CAD differs basically on the physiological

Fortunately enough, even if CAD is, by definition, severe sepsis, a good proportion of the patients are not in septic shock at presentation. This means that they are still in a physiological state to tolerate a definitive "classical" procedure. Standard surgical therapy for CAD has been to perform either an open or laparoscopic resection, followed by a primary anastomosis or a protected anastomosis or a terminal colostomy. The latter is still the most common procedure. In recent years, a less invasive approach has been used to fit patients with Hinchey III peritonitis. In these cases, a laparoscopic lavage and drainage (LLD) seem to be, according to a growing

In this chapter, we will not linger any longer on these previous strategies. We will focus only on the smaller group of patients with CAD who present with such an advanced derangement of their physiology that needs to be treated in a

Damage Control, in our view, is not merely a surgical technique. It is in fact, a strategy of treatment brought forward by a close collaboration between different specialties, among which surgery, intensive care (ICU) and anesthesia play a significant role. Thus, we will present the input on each of these specialties on the

We can think, out-of-the-book, abdominal emergencies as a devilish blend of dangerous ingredients. Diagnosing an acute abdomen is sorting out the different

We appreciate that there is a significant disparity in what can be used in different health systems. What is readily available in high-income countries, it is not (or is inexistent) in low-income countries. The authors' bias is to work in some of the best health systems in the world, at least according to the World Health Organization,

Ideally, we should be able to do it quickly, pragmatically, and in a cost-

We all know the signs and symptoms of a patient with acute diverticulitis. They usually have persistent moderate to severe abdominal pain with guarding and rebound tenderness located in the left lower quadrant or hypogastrium (Hinchey I–II), which turns to be diffused to all the abdominal cavity as the infec-

Nausea, vomiting, fever, and in some cases, dysuria can also be present in many

In modern and mature health care systems, patients with diffuse peritonitis and septic shock should be diagnosed straightforwardly with a CT abdomen-pelvis with intravenous contrast. We never stress enough to our trainees, and during our M&M, how a speedy diagnosis contributes to saving lives. Also, we are very adamant that a CT without IV contrast is a suboptimal examination in almost all the emergency clinical situations. Acute kidney injury (AKI) or chronic renal failure (CRF) are not, and should not be a contraindication to obtain a good quality CT scan. The quantity of literature on the safety of modern IV contrasts is vast and easily searchable

CT scan gives us all the information we need; such as free fluid vs. localized collection, the distribution of free air, and direct signs of diverticulitis. Not infrequently,

components from the mix to finally draw conclusions on its danger.

where almost everything is available 24/7/365.

tion is no longer localized (Hinchey III–IV).

**72**

patients.

in PubMed.

it informs us of other unknown conditions that could change the overall attitude such as multiple liver metastases, primary neoplasms of the large bowel or other organs, etc.

We agree that diagnosis is paramount, but treatment is our real goal. And treatment should start before diagnosis.

An acute abdomen is a diagnosis based on clinical examination. Sepsis should be considered as the primary cause of an acute abdomen until proven otherwise. Sepsis can be identified within minutes by recognizing hypotension, tachycardia, tachypnea, and oliguria. Blood tests (White Blood Cells and C-Reactive Protein) together with venous or arterial blood gases (lactates) can add crucial information towards the final diagnosis of sepsis. Are they septic? Are they in septic shock? Usually, in acute diffuse peritonitis, from diverticulitis or other causes as well, the answer is many times, yes, they are already in septic shock. Some Health Systems, like the United Kingdom's National Health System (NHS), introduced the "Sepsis-Six." The Sepsis-Six consists of three diagnostic and three therapeutic steps—all to be delivered within 1 h of the initial diagnosis of sepsis [7]:


Someone could argue that extremely sick patients, who are the ones who will require damage-control procedures, can be diagnosed on the spot by merely looking at them. They could also argue that a lot of scoring is useless and done only for scoring sake. We do not agree with them. It is imperative in our practice to assess the response to our treatment, and this can be done only if we have determined our starting point. We still use, as many other colleagues do, the concept and definitions of the "Surviving Sepsis Campaign: International Guidelines for the Management of Severe Sepsis and Septic Shock: 2012." We stress to our trainee the importance of assessing the patient and following their response to the treatment. Diagnosis at a glance also does not correlate with morbi-mortality, and it is not a common language used when dealing with other specialties, who would look upon your surgeon as a caveman.

We use the Sepsis definition, and the p-POSSUM score as a minimum to assess patient severity and surgical risk. We appreciate that P-POSSUM has been criticized, and possibly is not the best scoring tool available. Let us say that p-POSSUM is as bad as all the others available [7–9].

Septic patients are treated according to the Surviving Sepsis Campaign Bundle. Upon arrival, once the acute abdomen has been identified (again, it is a clinical diagnosis!), blood cultures are taken, and broad-spectrum antibiotics are started along with intravenous fluid replacement. For each hour of delay of antibiotic administration, there is a cumulative increase in mortality of 4%.

Which antibiotic should be administered is up to your hospital policies. Piperacillin/Tazobactam is the first choice in no-penicillin allergic patients in many hospitals.

Antibiotics, fluid, and oxygen are all you can do to start optimization and treatment. At the same time, you are now ready to pass the patient through the CT scan.

If you have done things correctly, you have lost no more than 30 min from arrival, and you should have been able to assess the problem (acute peritonitis), rule out other mimicking conditions (ruptured AAA clinically and laboratoristically is quite different) and evaluate the severity while starting the treatment. Ideally, a simple Chest X-ray should be performed during the initial assessment in the Accident & Emergency Department, to exclude free gas under the diaphragm (hollow viscous perforation). Furthermore, an abdominal ultrasound scan can exclude a AAA and give a piece of valuable information on possible free intraperitoneal fluid. Early involvement of a senior surgeon is crucial for the decision making and for coordinating with the other specialties.

An essential skill of the Emergency Surgeon should be interpreting CT scans. The Surgeon should be able to see the CT scan in real-time and seek advice from the Radiologist. Reviewing the scans together with the Radiologist, can give valuable information to the Surgeon and help him significantly to plan the strategy of the operation if needed. Since we are focusing on damage-control procedures, let us exclude all Hinchey I–II acute diverticulitis, and concentrate only on Hinchey III–IV, cases that are acute peritonitis. Usually, diagnosis of acute diffuse peritonitis is quite straightforward on a CT scan, even for a surgeon: free fluid, pneumoperitoneum, and fat stranding, alone or combined, are the key features. We see the CT scan, and we know that they will go to the OR for the source control.

Re-evaluation of the critically ill surgical patient is critical and essential. In many cases, the initial resuscitation has been adequate. The patient, hopefully, now has a good (or better) urinary output of at least 0.5 mL/Kg/h, is better perfused and does not require inotropic drugs. However, the patient still needs an emergency operation. In that case, the management options include a primary anastomosis with or without a prophylactic ileostomy or a Hartmann's procedure. That means that, most likely, a damage-control procedure is not needed.

Unfortunately, there are cases when the patient is not able to respond to resuscitation. The patient remains hypoperfused, oliguric/anuric, acidotic, coagulopathic, and often hypothermic. This sub-group of critically ill surgical patients is among the most challenging scenarios in emergency surgery. They are very often of old age, with multiple comorbidities and low reserves. They, unwillingly, form the vast majority of the mortality rate.

Yet, if you and the other members of the multidisciplinary team you are working with decide that invasive treatments are not futile, it is time to hurry up and do things properly.

In the real world, you have already spent at least 90 min: the patient has already been resuscitated all that it is advisable, and ideally, nothing can be added if source control is not obtained.

Just a couple of notes before entering the OR.

Remember the lethal triad in trauma: hypothermia, acidosis, and coagulopathy. We aim to fight those. Do not forget to actively warm your patients since they arrive to your observation. That means a warm environment and warm fluids. Also, if coagulation if deranged for the sepsis or in case they are on antiplatelet drugs or anticoagulants, you should involve the hematologist on-call as soon as possible, or use pre-existing protocols if available. It is not wise, although it is not infrequent, to find out an INR more than 2 just when you are ready to transfer them to OR. It is not a mortal sin, but it means more time to wait before source control, which, yes, increases mortality. Ways to correct the INR urgently in order to proceed with damage-control surgery include administering intravenous vitamin K, and transfusion of coagulation factor concentrates.

**75**

180 mg/dl [14].

volume status.

*Damage Control in Hinchey III and IV Acute Diverticulitis*

Now the patients need a general anesthesia. Anesthetists know very well that the anesthetic management of these patients requires always a rapid sequence induction

This consists of giving the patient supplementary O2 close to 100% for 30 s, asking to take three deep breaths as long as they are still conscious and collaborative. Subsequently, the hypnotic drug will be administered while another person assists by performing cricoid pressure. The cricoid pressure is maintained from the moment of induction until the intubation is completed. Applying pressure on the cricoid collapses the esophagus and prevents the passage of gastric contents to the larynx and respiratory tract. A fast-acting myorelaxant such as succinylcholine at a dose of 1 mg/kg iv or rocuronium at a dose of 1.2 mg/kg iv, will be administered just after the hypnotic drug. It will achieve a rapid opening of the vocal cords after approximately

Basic intraoperative monitoring will be achieved by ECG, non-invasive TA, O2 saturation by pulse oximetry, bispectral index (BIS), neuromuscular, core temperature, and hourly diuresis. Arterial canalization for invasive blood pressure monitoring and canalization is advised as well as obtaining a central venous route to administer large amounts of fluid therapy, vasopressors, blood products, or paren-

The primary anesthetic aim in these patients is to maintain or restore an adequate blood flow to guarantee an optimal O2 delivery to the tissues. Objectivedirected IV fluid therapy will be administered using dynamic hemodynamic variables (stroke volume variation—SVV, pulse pressure variation—PPV) to predict the response to fluid loading, guided by hemodynamic monitoring devices (CardioQ, PiCCo, and LiDCo) [11, 12]. If these devices were not available, static hemodynamic variables will be used with the following goals: maintaining central venous pressure >8 cm H2O; mean arterial pressure (MAP) >65–70 mmHg; diuresis >0.5 ml/kg/h; a venous saturation central (ScvO2) >70% or a mixed venous satura-

Unfortunately, static (HR, BP, and CVP) are not sensitive enough to predict a response to a fluid reposition and therefore are poor indicators of intravascular

Initial resuscitation with fluid therapy should be done with crystalloids. The administration of hydroxyethyl starch 130/0.4 should be avoided, as it appears to increase morbidity and mortality in these patients [13]. If the SSV or PPV are less than 10–15% with a PAM <65–70 mmHg despite the fluid challenge, or we do not have hemodynamic monitoring devices, but we have hypotension that does not respond to fluid therapy, vasopressors will be administered. Norepinephrine is the vasopressor of choice. Other options are adrenaline or vasopressin to reduce the dose of norepinephrine. Dobutamine will be administered in the presence of myocardial dysfunction or low cardiac output, or when signs of hypoperfusion persist

It is also necessary to maintain an adequate hydroelectrolytic and hemostatic balance, administering bicarbonate when essential and different hemostatic components to restore or maintain the coagulation. Coagulation can be assessed by standard tests, or by viscoelastic tests (VETs). The latter allow a treatment oriented

assessment of coagulation, and if available should be used as first choice. As for the transfusion of blood products, it is recommended to maintain hemoglobin levels between 7 and 9 g/dl, and glycemic levels should be kept below

*DOI: http://dx.doi.org/10.5772/intechopen.92669*

due to the high risk of bronchoaspiration.

15–20 s, allowing to pass the tracheal tube.

teral nutrition if required in the postoperative period [7, 10].

tion of O2 (SvO2) >65 mmHg and normalization of lactate.

despite adequate intravascular volume or MAP.

Now the ball is back in our court, the surgeon's.

**3. Operating room (OR)**
