Prevention and treatment of hospital-acquired conditions is as much a part of the care of the hospitalized patient as treatment of the primary diagnosis. The development of deep venous thromboses, stress-induced ulcers, and pressure ulcers can have a lasting, negative impact on a patient’s medical condition, requiring additional treatment and increasing the length of hospitalization. Also important in minimizing the length of hospitalization is fall avoidance, fluid and electrolyte management, and adequate nutrition. Infection control and isolation can limit the spread of multi-drug-resistant organisms, prompt removal of urinary catheters prevents catheter-associated urinary tract infections, and appropriate placement and site care of central venous catheters can prevent central line-associated bloodstream infections. Finally, the use of advanced care plans and early consultation of palliative care or hospice can assist in the care of the dying patient.

The hospital is a complex environment and a setting for the acute care of a patient’s medical needs. There are many players involved, including the patient, the patient’s family, physicians, nurse practitioners and physician assistants, nurses, nurse’s aids, physical and occupational therapists, phlebotomists, lab technicians, radiology technicians, transport staff, dieticians, pharmacists, housekeepers, social workers, nurse case managers, and the list goes on. Coordination of care and communication among these players are tantamount to improving patient experience and patient outcomes.

There is a newly recognized syndrome called post-hospital syndrome due to events related to being in the hospital environment. This relates to alterations in cognition, sleep deprivation and disruption of normal sleep cycles, malnutrition due to poor appetite in acute illness, and physical deconditioning from being in bed more than usual. This syndrome impacts a patient’s recovery, and prevention where possible in the hospital is crucial.¹

In addition to the acute care of the patient’s medical needs, there are innate risks to having an acute medical illness beyond the active medical needs. Many of these are preventable, and systems should be in place to help prevent such events including hospital-acquired infections, venous thromboembolism, pressure ulcers, injuries due to falls, and medication errors due to inadequate medication reconciliation.

When the time comes to decide if aggressive medical care should continue in a patient, we are not as prepared to talk with patients about end of life and may feel inadequately equipped to manage symptoms at the end of life. Patients may also have advanced directives that have been established or should be established in order to make their wishes known.

It is with these thoughts in mind that we have constructed this chapter.

In addition to management of his stroke, what conditions associated with hospitalization should be prevented?

1. 
   

   Venous thromboembolism

   
   
2. 
   

   Fall

   
   
3. 
   

   Pressure ulcers

   
   
4. 
   

   Healthcare-associated infections including catheter associated-urinary tract infections (CAUTI) and central line-associated bloodstream infections (CLABSI)

What medical care issues may need to be addressed?

1. 
   

   Intravenous hydration

   
   
2. 
   

   Nutrition

   
   
3. 
   

   Establishing goals of care

   
   
4. 
   

   End-of-life care

Deep venous thrombosis

Deep venous thromboses affect 1 in 1000 persons per year.² The risk factors for deep venous thrombosis (DVT) are many, including recent surgery and active malignancy (Table 3-1). Hospitalization for an acute medical illness is associated with an eightfold increased risk for venous thromboembolism (VTE).³

Consequences of DVTs include symptomatic DVT and pulmonary embolus (PE), fatal PE, chronic post thrombotic syndrome, and recurrent VTE.³

Diagnosing DVTs

Many tools are available to assist in diagnosis of acute DVTs, and an accurate history is essential. Once a history is taken, the Wells criteria can be used to stratify patients into high or low risk for DVTs.

After the clinical likelihood is determined, the D-dimer assay or venous ultrasound of the lower extremities is the next step in diagnosis. The D-dimer is a degradation product of cross-linked fibrin and is sensitive, though nonspecific, for the diagnosis of VTE. In low-risk patients, a negative D-dimer is enough to rule out the diagnosis of VTE. If the D-dimer assay is positive in a low-risk patient, the next recommended step is a venous ultrasound. In patients deemed high risk by Wells criteria, the next step in diagnosis is the venous ultrasound (Figure 3-1). It is important to note, however, that D-dimer has been tested in risk-stratifying patients for DVT in the ambulatory setting.⁴

Pharmacological prophylaxis of DVTs

There are many options available to prevent the formation of DVTs while in the hospital. Pharmacological thromboprophylaxis is associated with a reduction of 2 fewer fatal PEs per 1000 patients and 1 fewer symptomatic DVTs per 1000 in low-risk patients, 34 fewer in high-risk patients.²

Options for pharmacological prophylaxis include low-dose unfractionated heparin (LDUH) and low-molecular-weight heparin (LMWH). Heparin may be given 2 or 3 times per day; there is no compelling evidence of superiority for either choice. Both LDUH and LMWH are effective at preventing VTE and there is no benefit or harm for either for outcomes of DVT, PE, mortality, or heparin-induced thrombocytopenia (HIT).³

Nonpharmacological prophylaxis of DVTs

Besides chemical prophylaxis, there are nonpharmacological methods to prevent VTE. These methods include compression stockings, pneumatic compression devices, and venous foot pumps. There is no benefit for the prevention of DVT compared to heparin, although fewer DVTs are noted when the two are combined. Of course, these devices are only useful when they are operating appropriately, which usually requires the patient to be present in the room, sleeves applied and plugged in. The CLOTS3 trial has shown the efficacy of sequential compression devices (SCD) in preventing proximal and symptomatic DVTs, while also demonstrating the difficulties with patient adherence (only 60% in the study).⁵

Calf vein thromboses

Isolated calf vein thromboses also deserve a brief mention. As imaging modalities improve and their use increases, an increasing number of below-the-knee DVTs are being discovered. The routine use of anticoagulation in these cases results in increased bleeding complications. Absent risk factors for propagation (malignancy, immobility, and recent orthopedic surgery), both therapeutic anticoagulation and follow-up venous ultrasonography to assess propagation are viable options. There is no recommended time frame in which the ultrasound should be repeated.⁶

Pressure ulcers

A pressure ulcer is a localized injury confined to skin and possibly underlying tissues. They typically occur over bony prominences and can be due to shear forces over the area. Common areas include sacrum and heels.⁷ Stages of pressure ulcers are based on whether there is open skin and, if so, how deep is the breakdown. Pressure ulcers are contrasted by deep tissue injury, which is also damage to tissue due to pressure or shear, and are typically maroon or purple. Over time, deep tissue injury can be associated with skin breakdown.⁸ Care bundles should be utilized in order to standardize institutional practice around prevention and treatment of pressure ulcers and should involve a multidisciplinary team.⁹

Risk factors for pressure sores

Risk factors include immobility, difficulty with ambulation, history of stroke, fecal incontinence, low body weight, difficulty with independent feeding, impaired nutrition, and dry sacral skin. The majority occur in the acute care setting.¹⁰ Protective surfaces can help to prevent pressure ulcers and include specialized mattresses (eg, foam-filled or alternating-pressure mattresses). Repositioning patients every 2 hours is a common method utilized by care facilities for prevention. One large randomized controlled trial showed that nutritional supplementation reduced the risk of pressure ulcers.¹¹ Mixed data suggest that the use of moisturizing creams prevents pressure ulcers thought to be due to reduced friction of dry sacral skin. High-quality studies evaluating prevention are limited in number and more studies are needed to better inform prevention practice.

The Braden Scale

This is a commonly used, validated scale designed to identify patients at risk for developing pressure ulcers (Table 3-2). The scale assesses 6 domains: sensory perception, moisture exposure, mobility, nutrition, and risk for friction and shear. This is typically implemented by nursing. The lower the score, the higher the risk for developing pressure ulcers (score ranges from 6 to 23). This should be performed at admission and daily, if possible. The Norton Scale is another tool used to assess similar domains.⁹

Pressure ulcer stages

See also Table 3-2 and Figure 3-2.

• 
  

  Stage I: Nonblanchable erythema—may be more difficult to see in patients with dark skin tones; there is no skin breakdown in this stage.⁸

  
  
• 
  

  Stage II: Partial thickness—partial loss of dermis and is a shallow ulcer. May also present as a blister.

  
  
• 
  

  Stage III: Full-thickness skin loss—may see subcutaneous fat but not bone, tendon, or muscle; depth varies by location.

  
  
• 
  

  Stage IV: Full-thickness tissue loss—bone, tendon, or muscle is exposed; depth varies by location. These are at risk for bone infection or osteomyelitis.

  
  
• 
  

  Unstageable: Full-thickness tissue loss with unknown depth. These are obscured by slough and/or eschar and the stage is unknown until this is removed.

Treatment of pressure ulcers

Treatment of pressure ulcers depends on the location and the stage. Options include specialized mattresses, both nonpowered (eg, foam) and powered (eg, rotating beds). A review study found conflicting evidence behind using one over the other. The same study also found lack of evidence for nutritional interventions to promote healing with an exception for protein supplementation in patients with protein deficiency. Local wound care and dressings include those that are exudate absorbing, debriding, hydrating, antimicrobial, and other options. Adjunctive therapies such as light therapy, electric current, laser, and ultrasound have not been shown to be effective in promoting wound healing in this setting. Studies evaluating wound vacuum therapies are also inconclusive. Treating the underlying cause may be the most valuable.⁷

GI prophylaxis

In critically ill patients, hypoperfusion, acid hypersecretion, and overproduction of toxins can lead to irritation and disruption of the gastric mucosa, leading to ulcer formation. Mortality from stress ulcer-related bleeding is approximately 50% in critically ill patients.¹¹ Approximately 70% of patients on general wards receive stress ulcer prophylaxis without an appropriate indication.¹²