Surgical Critical Care 5

5

Surgical Critical Care

John T. Malcynski

Objectives

To describe the priorities in evaluating and treating a critically ill surgical patient:

• to identify immediate life-threatening situations and treat them accordingly.

• to discuss the systems approach to organ dysfunc- tion in the evaluation and treatment of the criti- cally ill surgical patient.

Cases

Case 1

A 28-year-old male unrestrained driver was involved in a head-on motor vehicle crash and found to have a grade III liver laceration that the trauma surgeon wants to manage nonoperatively. In addition, the patient is intubated due to a severe pulmonary contusion that has resulted in a significant hypoxemia. As the patient is brought into the intensive care unit (ICU) for you to manage, you note his skin is cool, pale, and mottled. As the nurse obtains initial vital signs, she tells you that his heart rate is 120 beats per minute and his blood pressure is 90/50 mm Hg.

Case 2

A 69-year-old woman has just arrived from the operating room after undergoing a sigmoid colectomy with Hartmann’s pouch and an end colostomy. As the surgeon drops off the patient in your care, he com- ments that there was a large amount of stool contamination in the abdomen that seemed to be present for several days. Due to a large amount of intraoperative fluids, the anesthesiologist decided to keep the patient intubated. You note that her heart rate is in the 100 s and her blood pressure is 80/45. Her skin is not noticeably cool to the touch.

82

Introduction

It is not uncommon for a medical condition or illness to involve mul- tiple organ systems. In addition to the primary anatomic insult and the problems that result, a cascade of physiologic derangements may occur that involve multiple, seemingly unrelated, organ systems. This usually is the case in the surgical critical care patient, where an initi- ating event, such as major trauma, burns, or infection, along with any premorbid conditions, results in a life-threatening situation that requires an understanding of complex physiologic interactions. The clinical condition characterized by severe dysfunction of multiple organ systems is termed multiple organ dysfunction system (MODS). The exact mechanisms of MODS have yet to be determined, but we do know that it is mediated by a series of complex interactions between intracellular components, such as cytokines, the neuroen- docrine system, and extrinsic products, such as endotoxin. The resul- tant condition is that of capillary leak, myocardial depression, and massive fluid balance changes. It is the task of the surgical intensivist, along with the facilities of the multidisciplinary ICU, to understand the interactions between the affected organ systems, dictate a course of support, and aid in the recovery of the patient.

As with any discipline, a thorough history and physical examina- tion are imperative in beginning to understand the process or processes at hand. This includes any premorbid conditions, such as heart or lung disease, as well as details of the latest insult that initiated the process at hand. Elements, such as injuries from a traumatic event, details of a surgical procedure, or the likely focus of infection, are helpful in deter- mining what steps need to be taken to provide appropriate support to the patient.

In addition, conditions that are immediately life threatening are addressed and treated in a systematic approach. As in other algo- rithms, such as Advanced Cardiac Life Support (ACLS) and Advanced Trauma Life Support (ATLS), following the ABC principle by con- ducting a primary survey (Table 5.1) ensures that the clinician ad- dresses the most critical conditions in the order of their potential to cause death.

Algorithm 5.1 provides a basic framework for the methodical ap- proach to the care of a patient in the ICU.

History and Physical Examination

History

As stated earlier, knowing the patient’s history (Table 5.2) is essential

for adequately treating a critically ill patient with multiple organ dys-

function. Premorbid conditions, such as a history of congestive heart

failure (CHF) or renal insufficiency, greatly affects the magnitude to

which a patient may respond to the illness and the therapies insti-

tuted to treat it. As in the trauma patient in Case 1, identification of all

injuries is crucial in helping avoid potentially hazardous therapeutic

measures, such as anticoagulation in a patient with a liver laceration or closed head injury. A list of preillness medications helps avoid pos- sible drug interactions from medications given in the ICU.

Physical Examination

In this technologic age of invasive monitoring and other advanced diagnostic modalities, it is easy to overlook the physical examination in the evaluation of the critically ill patient. By merely touching a patient and noting the temperature of the skin, one can diagnose that a patient is in shock and even determine the type of shock, such as in the patient with mottled, cool skin who is in hypovolemic shock. This is the situation in Case 1, where the cool, pale, mottled skin should alert the clinician that a derangement in the patient’s hemodynamics exists.

Table 5.1. Elements of the primary survey.

1. Airway Evaluation

Ensure airway is patent Problem

Obstruction from foreign body Anatomic obstruction (tongue)

Physiologic obstruction (vomitus, secretions) Therapy

Endotracheal/orotracheal intubation

Surgical airway (cricothyrotomy/tracheostomy) 2. Breathing

Evaluation

Ensure air is moving equally between both lungs Problem

Tension pneumothorax Hemothorax

Lung or lobar collapse Therapy

Needle thoracostomy Tube thoracostomy 3. Circulation Evaluation

Ensure adequate cardiovascular state Problem

Bleeding (GI hemorrhage, external bleeding source)

Shock—inadequate circulation for maintenance of cellular function (hemorrhagic, cardiogenic, septic, neurogenic)

Therapy

Adequate intravenous access (large-bore peripheral venous access, large-bore central venous access)

Fluid/blood product administration Invasive circulatory monitoring

Pharmacologic support (vasopressors/inotropes)

Control of primary source of blood loss

The loss of breath sounds over a lung field in a mechanically ventilated patient who experiences a sudden drop in blood pressure can reveal a tension pneumothorax. In this situation, waiting for further diagnostic tests may prove to be detrimental and may result in the patient’s death.

A systematic approach to the physical exam, especially when con- ducted the same way for each patient, ensures that no elements of the exam are neglected or missed. Depending on the examiner’s pref- erence, this usually is carried out anatomically from “head to toe” or using a systemic approach, such as commencing with the neurologic system and ending with the musculoskeletal system (Table 5.3).

Diagnostics and Management

Because critically ill patients frequently have dysfunction involving multiple organ systems, diagnostic measures and subsequent thera- pies are directed at the system involved. Not uncommonly, the treat- ment of one system has an effect on other organ systems. For example, improving cardiac performance also may improve renal func- tion. This complex nature of the interactions between organ systems adds an extra challenge to the intensivist. To provide a basic approach

Critically Ill Patient

History Present illness Comorbid conditions Previous surgery Allergies Medications

Physical exam

Primary survey

Airway Breathing Circulation

Address and correct each accordingly

Secondary survey (head to toe) Management with systems approach

Cardiovascular Pulmonary

Determine support required

Renal

Protect renal function as possible Determine etiology of renal dysfunction Determine type of shock

Invasive monitoring as needed

• • •

• •

Maximize preload (fluids/volume)

Provide adequate airway

Volume

mode Postrenal

Foley catheter

Prerenal

Renal Parenchymal Remove potential nephrotoxins

Hemodialysis if necessary Maximize intravascular volume

Pressure mode Initiate mechanical ventilation

Support throughout illness

Wean/remove support Afterload support (vasopressors)

Inotropic support

Algorithm 5.1. Evaluation and management of the critically ill patient.

to such problems encountered in the surgical critical care patient, this chapter discusses individual organ systems, focusing on pathophysio- logic changes, diagnosis, and treatment. Although virtually all organ systems, from the endocrine to the immunologic, are affected in some manner, those that are treated most commonly by the intensivist are the cardiovascular, pulmonary, and renal systems. Since this chapter is designed to provide a general overview of surgical critical care, these three organ systems are the primary focus of discussion.

Table 5.2. Important elements to be considered in the history.

Initiating insult

Blood loss and transfusions Foci of infection

Medical conditions Cardiac disease

Pulmonary dysfunction/chronic obstructive pulmonary disease

Hepatic disease/cirrhosis Renal insufficiency Bleeding disorders Peptic ulcer disease Surgical history

Coronary artery bypass graft Gastrointestinal procedures Medications

Allergies History of cancer

Table 5.3. A few of the elements of the physical exam that should be evaluated and documented.

General

Level of alertness Glasgow coma score Movement of extremities Head, ears, eyes, nose, and throat Scleral icterus

Mucous membranes Jugular venous distention Heart

Rhythm Rate Murmurs Lungs

Character of breath sounds Coarse

Rales Diminished Secretions

Abdomen Bowel sounds Diarrhea Distention

Blood (upper or lower) Skin

Turgor

Temperature

Peripheral edema

Capillary refill

Pulses

Cardiovascular Dysfunction

Shock is defined as the body’s inability to maintain adequate perfu- sion at the cellular level. Despite the etiology of the shock state, it is the failure of the cardiovascular system to provide this perfusion.

This state presents with hypotension, either by a systolic blood pres- sure (SBP) less than 90 mm Hg or a mean arterial pressure (MAP) less than 60 mm Hg. MAP can easily be calculated by the following formula:

where DBP is the diastolic blood pressure.

Details on the types of shock—hypovolemic/hemorrhagic, cardio- genic, septic, neurogenic, spinal, anaphylactic—are described in Chapter 7. Determination of the type of shock is very important because treatment strategies may differ depending on the etiology.

Each of the case presentations represents a patient in shock; however, the cause of each is different. The patient in Case 1 clearly is in hem- orrhagic/hypovolemic shock due to blood loss from his liver lacera- tion. The patient in Case 2 most likely is in septic shock from fecal peritonitis. Physical examination may give clues to the process at hand, but often this is not a reliable means by which to institute a therapy. It is in this situation that the technology of the ICU comes into play, and invasive hemodynamic monitoring can be very helpful.

As the term implies, invasive monitoring involves the placement of devices, such as catheters, into the body, whether it be a central vein, peripheral artery, or the heart itself. By using such devices, cir- culatory information, such as preload, afterload, and inotropy, as well as cardiac performance indicators, such as cardiac output, can be determined.

Preload

Preload refers to the load or tension on the myocardium when it begins to contract. Preload is determined by the quantity or volume of blood in the ventricle at the end of diastole, just before systole is to occur. When initiating cardiovascular support, preload should be max- imized prior to the initiation of vasopressors. This usually is facilitated by the use of invasive monitoring.

Central venous pressure (CVP) measures right-side cardiac pres- sures by way of a catheter placed into the superior vena cava (SVC), with the actual pressure obtained at the junction of the SVC and the right atrium (RA). The CVP measurements are accurate in determining preload provided certain conditions, such as right-sided heart failure, pericardial tamponade, or high positive end-expiratory pressures (PEEP) requirements while on mechanical ventilation, are not present.

If the CVP is low, one almost always can be assured that preload is not optimal.

Measurement of the pulmonary artery occlusion pressure (PAOP) is a more invasive monitoring technique that estimates the volume of the left ventricle. A catheter is inserted into the central venous system and passed into the right atrium, through the tricuspid valve, and into the

MAP 1

3 SBP DBP)/ DBP]

= [( -

right ventricle. From the right ventricle, the catheter is directed by the natural flow of blood into a dependent branch of the pulmonary artery (PA) until a balloon at the tip of the catheter eventually occludes flow from that artery. This also is known as wedging the balloon into the PA, thus the term wedge pressure. With the balloon occluding further flow in the PA branch, a stagnant column of blood results from the distal tip of the pressure transducer. Since no flow exists in this column of blood, one can assume that the pressure measured at the column is the same all along the column, which traverses the pulmonary capillary bed to the pulmonary veins into the left atrium (LA). Provided that there is no mitral valvular disease, such as mitral regurgitation, this pressure also should be accurate for the pressure of the left ventricle (LV). This point of measurement is obtained at end diastole, just before the LV contracts when the mitral valve is open. It then is possible to correlate this pres- sure with the volume of the LV. This correlation, however, only is pos- sible provided that the compliance—the ability of the ventricle to stretch adequately given the volume of blood it receives—of the LV is not impaired, as in the case of diastolic dysfunction, when the diseased ven- tricle is too stiff to adequately expand. In this case, high filling pressures may be seen by a small volume of blood in the ventricle. Case 1 and Case 2 both describe a patient with an inadequate preload. However, the etiology of each is quite different. The patient in Case 1 suffers from hypovolemia as a result of a massive hemorrhage, whereas the patient in Case 2 represents hypovolemia as a result of systemic inflammatory response syndrome (SIRS) with resultant intravascular fluid extravasa- tion. It is imperative that preload is maximized in each case, despite the different etiologies.

Afterload

Afterload is the pressure against which the ventricle must pump.

It typically is thought of as the resistance or tone that the arterial vasculature exhibits against the flow of blood as it travels through the vessel, where resistance is related to flow and pressure in the following equation:

Resistance = Pressure/Flow.

The resistance of the arterial vasculature, otherwise known as systemic vascular resistance (SVR), can be determined by the following formula:

SVR = MAP - CVP/CO

where CO is the cardiac output. Once preload is optimized, afterload is addressed by the administration of agents that either increase or decrease the vascular tone, depending on the type of shock present (Table 5.4). In cases in which vascular tone is decreased, such as septic shock, a-adrenergic receptor agonists, such as norepinephrine, epi- nephrine, phenylepherine, or dopamine, commonly are used. This is the situation with the patient in Case 2, who is exhibiting signs of septic shock secondary to the fecal contamination within her abdomen.

Hypovolemia is compounded with a loss of vascular tone, which

T able 5.4. V asoactive drugs and receptor activities for the treatment of shock. Systemic Coronary Blood vascular Cardiac Heart Isotrope Renal b lood Class and drug pressure resistance output rate Low-dose High-dose blood flow flow MvO

Alpha only ≠≠≠ ≠≠≠≠ ØØØ ØØØ ± ± ØØØØ ±≠≠ ≠ Phenylephrine Alpha and beta Norepinephrine ≠≠ ≠≠≠ ØØ Øر ≠ ≠ ØØØØ ≠≠ ≠≠ Epinephrine ≠± ≠± ≠≠ ≠≠≠ ≠≠ ≠≠≠ ر ≠≠ ≠≠≠ Dopamine ≠≠ ≠≠ ≠≠ ≠ ± ≠≠ ≠≠≠ ≠≠ ≠≠ Beta only Isoproterenol ≠± ØØ ≠≠≠≠ ≠≠≠≠ ≠≠≠ ≠≠≠≠ ± ≠≠≠ ≠≠≠≠ Dobutamine ØØ ØØØ ≠≠≠ ≠≠ ≠≠≠ ≠≠≠ ± ≠≠≠ ≠≠≠ Beta-blocker Propranolol +Ø ± ØØØ ØØØØ ØØ ØØØ Ø ØØ ØØØ Metoprolol ØØØ Ø ØØ ØØØ ØØ ØØØ ± ØØ ØØ Other Nitroglycerine ±Ø ØØ ≠≠ ± ± ± ±≠ Ø ØØ Hydralazine ØØØ ØØØ ≠≠ ≠≠ ± ± ±≠ Ø ØØ Prazosin ØØØ ØØ ≠≠ ± ± ± ±≠ Ø ØØ Nitroprusside ØØ ØØØ ≠≠≠ ±≠ ± ± ≠≠ ± ØØ Sour ce: Reprinted fr om Pettitt TW , Cobb JP . Critical car e. In: Doherty GM, Bauman DS, Cr eswell LL, Goss JA, Lairmor e TC, eds. The W ashi ngton Manual of Sur gery . Philadelphia: Lippincott W illiams & W ilkins, 1996. W ith permission fr om Lippincott W illiams & W ilkins.

ultimately will require vasoactive support. It should be stated again that it is vital to ensure that adequate intravascular volume or preload is attained prior to the initiation of vasopressors, since these agents can result in end-organ hypoxia and injury due to their vasoconstrictive properties. Organs particularly at risk are the kidneys and the gas- trointestinal tract.

Inotropy

Inotropy is the contractility of the myocardium and the force at which it occurs. According to Starling’s law, the contractility of the heart increases up to a critical point as the force against the myocardial fibers increases. A further increase of force causes a decrease of the contrac- tility. This force generated against the myocardial fibers is a result of blood entering the ventricle and causing it to expand. If, after preload is maximized, cardiac indices are less than desirable, manifested by a low stroke volume or cardiac output, inotropic agents may be ad- ministered to help improve cardiac performance. Dobutamine, a beta agonist, or the phosphodiesterase inhibitors amrinone and milrinone all increase cardiac contractility and thus cardiac output. It should be noted that as these agents increase the contractility of the myocardium, the oxygen requirement of the heart also increases and may worsen an already ischemic heart.

Pulmonary Dysfunction

The inability of a patient’s lungs to provide the body with adequate oxygen amounts in order to maintain cellular function (oxygenation) or the inability to adequately expel carbon dioxide (ventilation) is what is known as pulmonary dysfunction. When noninvasive means of support, such as supplemental oxygen administration, is adequate in compensating for this dysfunction, the term pulmonary insuffi- ciency is used. When more aggressive and invasive means of support are required, such as mechanical ventilation, the term pulmonary failure is used.

Etiology

There are many causes for pulmonary insufficiency and failure that involve all aspects of the respiratory system (Table 5.5). It is important to determine the etiology of the failure and look for potentially reversible causes, although support of the respiratory system is accom- plished essentially in the same way.

A major cause of pulmonary dysfunction in the surgical ICU is the

acute respiratory distress syndrome (ARDS). This condition com-

monly is seen in patients who have experienced severe trauma, are

septic, or have undergone a major operative procedure possibly requir-

ing a massive transfusion. This condition is the result of a systemic state

of inflammation known as SIRS, cited above, in which numerous

cellular components, such as cytokines and interleukins, along with

extrinsic mediators, such as bacterial lipopolysaccharide (LPS), act on

endothelial cells, causing an alteration in their permeability, which

results in a “leak” of intravascular components (both proteinaceous

and serous) into nonvascular spaces. This manifestation on the lung causes the alveoli to flood with water and protein to the extent that the alveoli are hindered markedly in their ability to transport oxygen into the blood. Although the lungs are affected and altered by SIRS, the disease process at hand usually is not a result of a primary lung problem, but it is merely an organ system where SIRS manifests.

Three criteria must be present to accurately define a condition as being ARDS (Table 5.6). The Po

/Fio

ratio of less than 200 denotes a severe hypoxia. A healthy individual breathing room air (Fio

= 0.21) should have a Po

of approximately 100 mm Hg, making the P/F ratio 476. A pulmonary artery wedge pressure less than 18 is necessary to rule out a cardiogenic etiology for the pulmonary edema. Pulmonary edema in the face of an elevated pulmonary copillary wedge pressure (PCWP) usually is a result of CHF and must be differentiated from ARDS. Finally, bilateral infiltrates on the chest x-ray (CXR) ensure that a pattern of pulmonary edema is present and that pneumonia is not all that is responsible for the hypoxia.

Treatment

Two separate processes, oxygenation and ventilation, must be consid- ered when planning to support the respiratory system. Each compo-

Table 5.5. Some common categories and causes of pulmonary dysfunction.

Neuromuscular

Brainstem injury/stroke Spinal cord injury Polio

Amyotrophic lateral sclerosis Mechanical

Airway obstruction (foreign body, trauma) Flail chest

Pneumothorax Diaphragmatic injury Parenchymal

Pneumonia

Pulmonary contusion

Acute respiratory distress syndrome Congestive heart failure

Miscellaneous Drug overdose Anaphylaxis

Table 5.6. Three criteria that must be present to accurately diagnose acute respiratory distress syndrome.

1. P

/Fi

ratio <200

2. Pulmonary capillary wedge pressure <18

3. Bilateral patchy infiltrates on chest x-ray

nent is relatively independent of the other but equally as important.

Oxygenation is the process in which atmospheric oxygenation is trans- ported to red blood cells via lung alveoli. Oxygen acts as the end recep- tor in the mitochondrial electron transport chain that is involved in cellular respiration. Ventilation is the process in which the lung releases carbon dioxide, a waste product from substrate metabolism, from the blood into the atmosphere.

The first decision to make in pulmonary management is whether to initiate support by way of mechanical ventilation. Typically, the parameters used in determining the need for such support are the following:

1. respiratory rate >30 breaths per minute 2. Pao

<60 mm Hg

3. Paco

>60 mm Hg

Severe tachypnea may cause excessive fatigue and exhaustion, while hypoxemia and hypercapnea reflect the inability to oxygenate or ven- tilate accordingly. Not all parameters need to be met in order to initi- ate mechanical ventilatory support.

The initial step in providing mechanical ventilation is securing an airway. This usually is accomplished by inserting a balloon-cuffed tube into the trachea by way of a nasotracheal or orotracheal route. This tube is then attached to connection tubing that is then connected to the ventilator.

Next, the ventilator is adjusted to the desired settings. The inten- sivist has several different ventilatory modes he may employ in meeting his objective. These modes primarily describe the means by which a breath is delivered from the machine to the patient, either by volume or by pressure. When a breath is delivered by volume, a des- ignated volume is set on the ventilator, and the ventilator delivers that set amount of gas. A pressure mode delivers an amount of gas into the lungs up to a given pressure that is set on the ventilator. The volume of gas administered is determined by how compliant the lungs are and how much they can stretch with a given force of air. Compliance is cal- culated as the change in volume divided by the change in pressure:

dV/dP

where normal is 100 mL/cm H

O. A lung that is very sick may have a low compliance (<20) and therefore be very stiff. A pressure limit of 35 cm water may generate only a tidal volume of 200 cc, whereas the same pressure limit of 35 cm would generate 800 cc in a healthy lung.

The advantage of a pressure control is that, by limiting the pressure to which the lung will be subjected, there is less of a chance of causing injury to the lung, known as barotrauma, from excessive airway pres- sures that sometimes may result when using a volume mode.

The next decision to make is determining whether mandatory

breaths are to be administered or whether only supported breaths are

required. It is possible even to have a combination of each. Mandatory

breaths, as the term implies, involves setting a given number of breaths

that the patient will receive. This number may be the only breaths the

patient receives or may be in addition to breaths that the patient con- tributes, with or without additional support from the ventilator. Sup- ported breaths are initiated by the patient, usually with a determined level of support supplied or assisted by the ventilator.

When a suitable ventilatory mode is determined according to the patient’s clinical status, the goal is to achieve appropriate minute ven- tilation—the volume of gas exhaled in 1 minute—in order to maintain a eucapnic state. This is accomplished by setting the desired tidal volume and respiratory rate. Tidal volume usually is calculated to be 10 to 12 mm per Kilogram of body weight. A recent exception is in the case of a patient with ARDS, where prospective studies have shown that 6 to 8 mm Hg/g body wt. may have a protective effect on the lung and reduce overall mortality. Next, a respiratory rate is determined to achieve a minute ventilation of 8 to 12 L/min. An arterial blood gas is drawn 30 minutes after support has been initiated, and the Pco

is eval- uated. The tidal volume or respiratory rate is adjusted accordingly to bring the Pco

to a desirable level. The more common ventilatory modes and their comparisons are listed in Table 5.7.

After the desired ventilatory mode and parameters are chosen, the priority of oxygenating the patient is addressed. This is accomplished by selecting a level for both the fractional inspired oxygen (Fio

) and PEEP. The Fio

is the percentage of oxygen mixed with nitrogen that is to be delivered to the patient. The ranges are from atmospheric oxygen concentration of 21% or 0.21 to supplying 100% or 1.0 oxygen. Typi- cally, the Fio

is started at 1.0 and then titrated to a level to maintain oxygen saturation between 92% and 95%.

A person with a minimal alveolar-arterial (A-a) gradient usually will end up with an Fio

set at 0.4; PEEP, which is the residual pressure in the alveoli at the end of expiration, is added to help prevent atelecta- sis. With a minimal A-a gradient, PEEP usually is set at 5 cm H

O, which also is known as physiologic PEEP. Higher levels of PEEP can be added to facilitate oxygenating the patient, especially when a large diffusion gradient exists, as in ARDS. It is thought that PEEP helps to improve the functional residual capacity (FRC) of the lung and aids in recruiting unused alveoli. In addition, PEEP may play a role in thin- ning out the thick proteinaceous fluid layer in the alveoli, thus pro- moting oxygen diffusion across the basement membrane of the alveoli.

Disadvantages of PEEP, especially at higher levels in the 20- to 30-cm H

O range, include barotrauma to the airways, resulting in a tension pneumothorax and a decline in cardiac output as a result of decreased cardiac filling from compression of the pulmonary veins from such high intrathoracic pressures. In cases of severe life-threatening hypoxia, other ventilator strategies can be employed, such as reversing the inspi- ratory to expiratory (I : E) ratio, thus allowing a longer time for oxygen to diffuse across diseased basement membrane. This strategy, however, involves an unnatural breathing pattern and usually requires that a patient be sedated heavily or even chemically paralyzed in order to allow this ventilatory mode to be effective.

Ventilatory support is continued throughout the patient’s acute

illness. As the patient resolves the illness at hand, the intensivist is

T able 5.7. Conventional ventilator modes. Mode Description Advantages Disadvantages Uses A. V olume-limited Set tidal volume; peak Ensures adequate tidal Barotrauma in those inspiratory pressure volume with very poor lung varies compliance 1. Assist/control Both spontaneous (patient- Minimal work of breathing Easy for patient to W eak, heavily sedated, (A/C) initiated, “assisted”) and hyperventilate or paralyzed (“controlled”) breaths Makes assessment of have same tidal volume ventilatory muscle strength dif ficult to evaluate 2. Intermittent T idal volume of machine- Allows gradual decrease No support for Often used in mandatory initiated (“mandatory”) of support by decreasing spontaneous breaths combination with ventilation breaths set; no ventilator rate of mandatory PSV for weaning (IMV) support for spontaneous breaths breaths B. Pressure-limited Set peak inspiratory Decreased risk of Does not ensure tidal pressure; tidal volume barotrauma volume varies 1. Pressure Inspiratory pressure and Inverse ratio ventilation Requires heavy sedation Patients with very poor control rate set (IR V); increased alveolar and/or paralytics lung compliance ventilation “recruitment” (PCV) 2. Pressure Inspiratory pressure set; Most comfortable of the Increased risk of A wake patients; often support no rate conventional modes hypoventilation used in combination ventilation with IMV for weaning (PSV) Sour ce: Reprinted fr om Cobb JP . Critical car e: a system-oriented appr oach. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Sur gery: Basic Science and Clinical Evidence. New Y ork: Springer -V erlag, 2001, with permission.

able to decrease the amount of work that is being accomplished by the ventilator as well as the amount of oxygen required.

Discontinuation of Mechanical Ventilation

There are as many strategies employed to wean a patient off the ven- tilator as there are ventilatory modes. The most common involves the gradual decrease in the minute ventilation supported by the machine, allowing the patient to supply the difference. This is done either by gradually decreasing the number of mandatory breaths given to the patient or decreasing the amount of pressure supplied to the patient during the supported breaths. Several prospective studies have evaluated these popular strategies and can be reviewed in Table 5.8.

Once it is decided that a patient has a good chance of discontinued ventilatory support, that is, is on minimal assisted settings with a low Fio

while maintaining an acceptable minute ventilation without being fatigued from tachypnea, consideration is made regarding removing the breathing tube or extubating the patient. Traditional parameters use such indices as the spontaneous tidal volume and the vital capacity a patient can generate as well as the degree of negative pressure or neg- ative inspiratory force (NIF) a patient can generate. Recently, an index has been used to predict the success of keeping a patient off the venti- lator once extubated. This index is known as the Rapid Shallow Breath- ing Index (RSBI) and is determined by the number of breaths in 1 minute divided by the tidal volume of each breath (f/Vt). Patients with an RSBI less than 100 have a high rate of success (in the order of 80%+) in remaining extubated.

Table 5.8. Prospective, randomized, controlled clinical trials comparing strategies to wean mechanical ventilation (level I evidence).

Duration of Duration of Authors and No. of ventilation before ventilation after

reference patients Comparisons randomization randomization Conclusion Brochard 109 IMV vs. PSV vs. 17 vs. 11 vs. 9.9 vs. 5.7 vs. PSV best

et al.

T-piece 14 days 8.5 days

Esteban 130 IMV vs. PSV vs. 6.5 vs. 10.8 vs. 5 vs. 4 vs. 3 days T-piece best

et al.

T-piece 11.5 days

Ely et al.

300 Routine vs. daily 3 vs. 2.5 days 3 vs. 2 days Daily T-piece

T-piece better

Kollef et al.

357 Routine vs. 2.4 vs. 1.7 days 1.5 vs. 1.2 days Protocol better protocol

a

Brochard L, Rauss A, Benito S, et al. Comparison of three methods of gradual withdrawal from ventilatory support during weaning from mechanical ventilation [see comments]. Am J Respir Crit Care Med 1994;150(4):896–903.

b

Esteban A, Frutos F, Tobin MJ, et al. A comparison of four methods of weaning patients from mechanical venti- lation. Spanish Lung Failure Collaborative Group [see comments]. N Engl J Med 1995;332(6):345–350.

c

Ely EW, Baker AM, Dunagan DP, et al. Effect on the duration of mechanical ventilation of identifying patients capable of breathing spontaneously [see comments]. N Engl J Med 1996;335(25):1864–1869.

d

Kollef MH, Shapiro SD, Silver P, et al. A randomized, controlled trial of protocol-directed versus physician-directed weaning from mechanical ventilation [see comments]. Crit Care Med 1997;25(4):567–574.

Source: Reprinted from Cobb JP. Critical care: a system-oriented approach. In: Norton JA, Bollinger RR, Chang AE,

et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001, with permission.

Renal Dysfunction

Renal dysfunction is not a rare occurrence in the surgical ICU. Associ- ated many times with SIRS and multisystem organ failure (MSOF), renal dysfunction, which may lead to renal failure, carries a substan- tial mortality rate in ICU patients, approaching 50% in some investi- gations. It is this fact that encourages the surgical intensivist to attempt to “protect” the kidneys as much as possible during a critical illness.

This usually is accomplished by maximizing renal perfusion while simultaneously minimizing any potential nephrotoxins.

Early signs of renal dysfunction are characterized by a prolonged decrease in urine output and a rise in the blood urea nitrogen (BUN) and serum creatinine. Late signs of frank renal failure include fluid overload, hyperkalemia, platelet dysfunction, acidosis, and even pericardial effusion. When renal dysfunction is first suspected, all eti- ologies should be sought out and corrected, if possible. This usually is thought out anatomically by addressing the three components of renal function, namely, prerenal, renal (parenchymal), and postrenal.

The prerenal component regards the perfusion to the kidneys. Inad- equate renal perfusion results in renal hypoxia and can lead to acute tubular necrosis (ATN). Prolonged hypotension and hypovolemia are the primary causes for a prerenal etiology of renal failure. Tests that may help determine a prerenal cause include measurement of the urine sodium or calculation of the fractional excretion of sodium (FE Na).

A urine sodium less than 10 mEq/L sodium implies sodium conserva- tion, with functional renal tubules that can reabsorb salt, and points to a prerenal picture, while a urine sodium greater than 20 mEq/L usually represents the inability of injured renal tubules to conserve sodium, thus wasting salt. The fractional excretion of sodium tends to be a more reliable test and is determined by obtaining urine and serum levels of sodium and creatinine and using the following formula:

(Urine Na ¥ Serum Cr/Serum Na ¥ Urine Cr) ¥ 100

A value less than 1 implies prerenal syndrome, while a value greater than 1 implies a parenchymal etiology.

Prerenal failure is treated by maximizing filling pressures and intravascular volume, ensuring that renal perfusion is optimum. Judi- cious use of vasopressors is warranted, however, because, while they can increase blood pressure, they can cause a profound constriction of the renal arteries and actually decrease the perfusion to the kidneys.

Drugs such as dopamine and furosamide do increase urine output, but

there is no scientific proof that these agents prevent or improve renal

function, nor have they been shown to improve overall survival when

used in such situations. It is clear that nonoliguric renal failure

(>500 cc urine/day) carries a more favorable prognosis with respect to

return of renal function and overall survival than does oliguric renal

failure (<500 cc urine/day), but conversion of oliguric renal failure to

nonoliguric renal failure using dopamine or furosamide has no effect

on either renal function or survival.

Renal parenchymal failure involves the kidney and the actual renal tubules. This usually is referred to as ATN, which entails actual cellular death of the nephrons and loss of viable kidney tissue. See Table 5.9 for the common causes of ATN.

Treatment for this type of renal failure consists of maximizing renal perfusion and removing any potential nephrotoxins. The natural history of ATN occurs over a period of 10 to 14 days. This is noted by a serial increase in the BUN and serum creatinine. Resolution of ATN is characterized by an eventual plateau of the serum creatinine until the level begins to fall. If by day 14 the creatinine level does not plateau, the chances of renal function returning are very slim. Finally, a postre- nal etiology for renal dysfunction should be ruled out. Postrenal causes are a result of an obstruction of urine at the level of the ureters or below that results in an oliguric or anuric state. An increase of BUN and serum creatinine also may be discovered.

Although less common than the previous two types of renal dys- function, on occasion postrenal dysfunction may be the only explana- tion for the problem. Bilateral ureteral obstruction or bladder outlet obstruction from a clogged urethral catheter are the more common eti- ologies. Simply changing the urethral catheter may be all that is required to resolve the issue. An abdominal ultrasound may be helpful in determining if hydroureters or hydronephroses are present.

The patients in both Case 1 and Case 2 are susceptible to the devel- opment of renal failure, despite the difference in their physiologic state.

Each has the potential for renal hypoperfusion that can lead to ATN. It is crucial for the clinician to make every effort to maintain renal per- fusion while avoiding potential nephrotoxins, if possible.

Occasionally in the ICU, a patient requires hemodialysis as a result of the manifestations of the renal failure. These manifestations usually are life threatening and require immediate attention. Here is a list of the emergency indications requiring hemodialysis in the ICU:

Volume overload/CHF Severe acidosis

Hyperkalemia

Uremia/platelet dysfunction/bleeding

Continuous veno-veno hemofiltration and dialysis (CVVHD) is a form of hemodialysis performed in some tertiary centers. As the term implies, this technique involves the continuous circulation of blood

Table 5.9. Common causes of acute tubular necrosis.

Prolonged hypotension and ischemia IV x-ray contrast

Nephrotoxic drugs (aminoglycosides, furosamide) Rhabdomyolysis/myoglobin

Transfusion reaction

Hemolytic-uremic syndrome

Hepatorenal syndrome

through a specially designed hemodialysis machine that removes a smaller amount of fluid from the patient on an hourly basis. It also is equipped with a membrane that can address the metabolic conse- quences of ATN. The advantage of CVVHD is that smaller amounts of fluid can be removed over a longer period of time, resulting in less drastic fluid shifts for the patient. Disadvantages include systemic anti- coagulation, which keeps the venous lines from clotting, and the need for specialized personnel.

Summary

The critically ill surgical patient often has multiple organ system dys- function, which requires the surgical intensivist to use a methodical approach in treating such patients. A thorough history and a thorough physical examination are essential initial steps in the management scheme. Frequently, invasive monitoring techniques are required to supply additional information about the patient’s status and to help guide therapeutic maneuvers. It is important to realize that, despite using the systems approach for the management of the critically ill, treatment of one system has an effect on the others, resulting in both positive and negative repercussions.

Selected Readings

Bernard GR, Artigas A, Brigham KL, et al. Report of the American-European consensus conference on ARDS: definitions, mechanisms, relevant outcomes and clinical trial coordination. The Consensus Committee. Intensive Care Med 1994;20:225–232.

Bone RC, Balk RA, Cerra FB, et al. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physi- cians/Society of Critical Care Medicine. Chest 1992;101:1644–1655.

Cobb JP. Critical care: a system-oriented approach. In: Norton JA, Bollinger RR, Chang AE, et al., eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001:277–290.

Fink MP. Monitoring techniques and complications in critical care. In: Norton JA, Bollinger RR, Chang AE, et al., eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001:291–303.

Kollef MH, Schuster DP. The acute respiratory distress syndrome. N Engl J Med 1995;332:27–37.

Marshall JC. Risk prediction and outcome description in critical surgical illness.

In: Norton JA, Bollinger RR, Chang AE, et al., eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001:305–320.

Moore FA, Moore EE. Evolving concepts in the pathogenesis of postinjury mul-

tiple organ failure. Surg Clin North Am 1995;75:257–277.