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What organ goes first in organ failure?

Multiple Organ Dysfunction Syndrome

Hi, and welcome to this video about multiple organ dysfunction syndrome! We’re going to look at an overview of the disease, the signs and symptoms, diagnosis, and management. Let’s get started!

Multiple organ dysfunction syndrome (MODS) refers to an acutely ill patient that has progressive organ dysfunction, in which homeostasis cannot be maintained without intervention. It is a process rather than a single event, and it is at the severe end of illness severity of both infectious and noninfectious conditions.

It can be classified as primary or secondary:

  • Primary MODS is the result of a definite insult to an organ, in which organ dysfunction occurs early and can be directly attributed to the insult itself.
  • Secondary MODS refers to organ failure that occurs as a result of the patient’s response to an illness, often sepsis, rather than a direct insult to the organ.

Our focus today will be on secondary MODS, caused by sepsis. Sepsis is a clinical syndrome in which a severe infection becomes complicated and is characterized by systemic inflammation and widespread tissue injury. The clinical process usually begins with infection, which can lead to sepsis and then organ dysfunction.

Symptoms of sepsis are typically nonspecific and include fever and chills, along with more specific symptoms of malaise, fatigue, confusion, or anxiety. Since there is a continuum of severity from sepsis to septic shock to MODS, the specific symptoms exhibited depend on where the patient falls on the continuum. Look for signs of a localized infection. Assessment of the patient’s overall condition usually reveals an acutely ill, toxic appearance in patients with serious infections. Tachypnea is common, as well as tachycardia with an increased pulse pressure. In the early stages of sepsis, cardiac output is well maintained or even increased, but as sepsis progresses, stroke volume and cardiac output fall. Patients begin to have poor distal perfusion, including cool extremities, cool skin, and delayed capillary refill.

Localized infections often present with the following physical signs:

  • Central nervous system infection – exhibits profound depression in mental status.
  • Head and neck infections – cause inflamed or swollen tympanic membranes, sinus tenderness, stridor, pharyngeal exudates, or cervical lymphadenopathy.
  • Chest and pulmonary infections – cause localized rales or lung consolidation.
  • Cardiac infections – cause a regurgitant valvular murmur.
  • GI infections – exhibit abdominal tenderness, rectal tenderness, or swelling.
  • Pelvic and GU infections – cause pelvic or adnexal tenderness, and/or renal tenderness.
  • Bone and soft tissue infections – exhibit redness, edema, and tenderness.
  • Skin infections – often show up as petechiae and purpura.

A scoring system is utilized to assess the severity of organ dysfunction in patients who are critically ill from sepsis. SOFA (Sequential Organ Failure Assessment) uses simple measurements of major organ function to calculate a severity score, with the highest score most predictive of mortality.

SOFA Score for risk of dying from sepsis

The SOFA severity score is based on the following organ function measurements:

  • Respiratory system – the ratio of PaO2 to FiO2
  • Cardiovascular system – the amount of vasoactive medicine required to prevent hypotension
  • Hepatic system – the bilirubin level
  • Coagulation system – the platelet concentration
  • Neurologic system – the Glasgow coma score
  • Renal system – the serum creatinine or urine output

The SOFA score is used as a tool to facilitate the identification of patients at risk of dying from sepsis.

Diagnosis of MODS involves laboratory tests to identify sepsis in order to assess the general hematologic and metabolic condition of the patient.

  • A CBC with differential is necessary to evaluate oxygen delivery in shock, and with persistent sepsis, the platelet count will fall. The White Blood Cell count and differential can predict the existence of a bacterial infection.
  • A complete metabolic panel (CMP) will assess serum electrolytes, as well as renal and hepatic function.
  • Serum lactate assesses tissue hypoperfusion – elevated levels indicate that significant tissue hypoperfusion exists, signaling a worse degree of shock and higher mortality.
  • PT and aPTT will assess coagulation status and evidence of coagulopathy would require additional tests to detect disseminated intravascular coagulation (DIC).
  • Blood cultures can be used to diagnose intravascular infections and infections of indwelling intravascular devices.
  • A urinalysis and urine culture should be done since urinary infection is a common source of sepsis, especially in the elderly.
  • Secretions or tissue of Gram stain and culture should be obtained from sites of potential infection.

Various imaging methods are also used to diagnose focal infections and evaluate complications of sepsis and septic shock.

  • A chest x-ray can diagnose pneumonia infiltrates. X-ray can also help identify a deep soft tissue infection.
  • Ultrasound is used when a biliary tract infection is suspected as the source of sepsis.
  • Computed tomography (CT) is utilized when assessing for an intra-abdominal abscess or a retroperitoneal source of infection. A CT scan of the head should be obtained when there is increased intracranial pressure, suspected focal mass lesions, or before lumbar puncture when meningitis is suspected.
What is the strongest organ?

There are two forms of multiple organ dysfunction syndrome. In both, the development of acute lung injury (ALI) or ARDS is the earliest manifestation.

In the more common form of MODS, the lungs are the predominant, and often the only organ system affected until very late in the disease. Patients often present with a primary pulmonary disorder, such as pneumonia, contusion, aspiration, near drowning, hemorrhage, exacerbation of COPD, or pulmonary embolism. When the lung disease progresses, encephalopathy or mild coagulopathy may occur, persisting for 2-3 weeks. At this point, the patient either begins to recover or progresses to a sudden dysfunction in another organ system. Once another major organ dysfunction occurs, these patients frequently do not survive.

The second form of MODS presents with the causative source in organs other than the lungs – most commonly intra-abdominal sepsis, pancreatitis, extensive blood loss, or vascular catastrophes. ARDS still develops early and dysfunction in other organ systems also develops much sooner than in the first form of MODS. For several weeks, patients remain in a pattern of compensated dysfunction, at which time they either recover or deteriorate further and die.

When we look at treatment for multiple organ dysfunction syndrome, it is not so much a syndrome to be treated, but a complication to be prevented. Treatment begins with treating septic shock before it turns into MODS. The goals of treatment include:

  • Resuscitate the patient from septic shock, correct hypoxia, hypotension, and impaired tissue oxygenation.
  • Identify the source of infection and treat it with antimicrobial therapy, surgery, or both.
  • Maintain adequate organ system function, guided by cardiovascular monitoring, and interrupt the pathogenesis of MODS.

Addressing these goals involves:

  • Early recognition of septic shock, which requires identifying signs of the systemic inflammatory response syndrome (SIRS) – mental changes, hyperventilation, hyperthermia or hypothermia, and an abnormal WBC count – along with the existence of a potential source of infection.
  • Early cardiorespiratory stabilization and continued hemodynamic support
  • Early and adequate antibiotic therapy
  • Maintain blood glucose levels less than 150 mg/dL (milligrams per decilitre)
  • Proper ventilator management with low tidal volume in patients with ARDS.

The road to recovery is often long and challenging for patients who survive sepsis and MODS. Patients may have physical, emotional, and cognitive consequences after discharge from the hospital. These patients also have a higher risk of repeat sepsis episodes. Aggressive rehabilitation programs, including psychological treatments, may be helpful.

Now that we’ve learned all about MODS, let’s go over a few questions for review.


1. Organ failure that occurs as a result of the patient’s response to sepsis refers to

  1. SIRS
  2. Primary MODS
  3. Secondary MODS
  4. Septic shock

Show Answer
If you chose C, secondary MODS, you are correct!

2. The scoring system used to assess the severity of organ dysfunction in patients who are critically ill from sepsis is called the

  1. BPP (Biophysical profile) Score
  2. SOFA (Sequential Organ Failure Assessment)
  3. AN (Care Assessment Need) Score
  4. GAF (Global Assessment of Functioning) Scale

Show Answer
If you chose B, Sequential Organ Failure Assessment, you are correct!

That’s all for now! Thanks for watching and happy studying!


by Mometrix Test Preparation | This Page Last Updated: January 31, 2023

Multiple organ dysfunction syndrome

Multiple organ dysfunction syndrome (MODS) is altered organ function in an acutely ill patient requiring medical intervention to achieve homeostasis.

Although Irwin and Rippe cautioned in 2005 that the use of «multiple organ failure» or «multisystem organ failure» should be avoided, [1] both Harrison’s (2015) and Cecil’s (2012) medical textbooks still use the terms «multi-organ failure» and «multiple organ failure» in several chapters and do not use «multiple organ dysfunction syndrome» at all.

There are different stages of organ dysfunction for certain different organs, both in acute and in chronic onset, whether or not there are one or more organs affected. Each stage of dysfunction (whether it be the heart, lung, liver, or kidney) has defined parameters, in terms of laboratory values based on blood and other tests, as to what it is (each of these organs’ levels of failure is divided into stage I, II, III, IV, and V). The word «failure» is commonly used to refer to the later stages, especially IV and V, when artificial support usually becomes necessary to sustain life; the damage may or may not be fully or partially reversible.

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Signs and symptoms [ edit ]

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Cause [ edit ]

The condition results from infection, injury (accident, surgery), hypoperfusion and hypermetabolism. The primary cause triggers an uncontrolled inflammatory response. [ citation needed ]

Sepsis is the most common cause of multiple organ dysfunction syndrome and may result in septic shock. In the absence of infection, a sepsis-like disorder is termed systemic inflammatory response syndrome (SIRS). Both SIRS and sepsis could ultimately progress to multiple organ dysfunction syndrome. In one-third of the patients, however, no primary focus can be found. [1] Multiple organ dysfunction syndrome is well established as the final stage of a continuum: SIRS + infection → sepsis → severe sepsis → Multiple organ dysfunction syndrome. [ citation needed ]

Currently, investigators are looking into genetic targets for possible gene therapy to prevent the progression to multiple organ dysfunction syndrome. Some authors have conjectured that the inactivation of the transcription factors NF-κB and AP-1 would be appropriate targets in preventing sepsis and SIRS. [2] These two genes are pro-inflammatory. They are essential components of a normal healthy immune response, however, so there is risk of increasing vulnerability to infection, which can also cause clinical deterioration. [ citation needed ]

Pathophysiology [ edit ]

A definite explanation has not been found. Local and systemic responses are initiated by tissue damage. Respiratory failure is common in the first 72 hours. Subsequently, one might see liver failure (5–7 days), gastrointestinal bleeding (10–15 days) and kidney failure (11–17 days). [1]

Gut hypothesis [ edit ]

The most popular hypothesis by Deitch to explain MODS in critically ill patients is the gut hypothesis. [3] Due to splanchnic hypoperfusion and the subsequent mucosal ischaemia there are structural changes and alterations in cellular function. This results in increased gut permeability, changed immune function of the gut and increased translocation of bacteria. Liver dysfunction leads to toxins escaping into the systemic circulation and activating an immune response. This results in tissue injury and organ dysfunction. [1]

Endotoxin macrophage hypothesis [ edit ]

Gram-negative infections in MODS patients are relatively common, hence endotoxins have been advanced as principal mediator in this disorder. It is thought that following the initial event cytokines are produced and released. The pro-inflammatory mediators are: tumor necrosis factor-alpha (TNF-α), interleukin-1, interleukin-6, thromboxane A2, prostacyclin, platelet activating factor, and nitric oxide. [1]

Tissue hypoxia-microvascular hypothesis [ edit ]

As a result of macro- and microvascular changes insufficient supply of oxygen occurs. Hypoxemia causes cell death and organ dysfunction. [1]

Mitochondrial DNA hypothesis [ edit ]

According to findings of Professor Zsolt Balogh and his team at the University of Newcastle (Australia), mitochondrial DNA is the leading cause of severe inflammation due to a massive amount of mitochondrial DNA that leaks into the bloodstream due to cell death of patients who survived major trauma. [ citation needed ]

Mitochondrial DNA resembles bacterial DNA. If bacteria triggers leukocytes, mitochondrial DNA may do the same. When confronted with bacteria, white blood cells, or neutrophil granulocytes, behave like predatory spiders. They spit out a web, or net, to trap the invaders, then hit them with a deadly oxidative blast, forming neutrophil extracellular traps (NETs). [ citation needed ]

This results in catastrophic immune response leading to multiple organ dysfunction syndrome. [4] [5]

Integrated hypothesis [ edit ]

Since in most cases no primary cause is found, the condition could be part of a compromised homeostasis involving the previous mechanisms. [1]

Diagnosis [ edit ]

The European Society of Intensive Care organized a consensus meeting in 1994 to create the «Sepsis-Related Organ Failure Assessment (SOFA)» score to describe and quantitate the degree of organ dysfunction in six organ systems. Using similar physiologic variables the Multiple Organ Dysfunction Score was developed. [1]

Four clinical phases have been suggested: [ citation needed ]

  • Stage 1: the patient has increased volume requirements and mild respiratory alkalosis, which is accompanied by oliguria, hyperglycemia and increased insulin requirements.
  • Stage 2: the patient is tachypneic, hypocapnic and hypoxemic; develops moderate liver dysfunction and possible hematologic abnormalities.
  • Stage 3: the patient develops shock with azotemia and acid-base disturbances; has significant coagulation abnormalities.
  • Stage 4: the patient is vasopressor dependent and oliguric or anuric; subsequently develops ischemic colitis and lactic acidosis.

Definition [ edit ]

Multiple dysfunction syndrome is the presence of altered organ function in acutely ill patients such that homeostasis cannot be maintained without intervention. It usually involves two or more organ systems. It calls for an immediate intervention. [1]

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Management [ edit ]

At present, there is no drug or device that can reverse organ failure that has been judged by the health care team to be medically and/or surgically irreversible (organ function can recover, at least to a degree, in patients whose organs are very dysfunctional, where the patient has not died; [ citation needed ] and some organs, like the liver or the skin, can regenerate better than others),- with the possible exception of single or multiple organ transplants or the use of artificial organs or organ parts, in certain candidates in specific situations. Therapy, therefore, is usually mostly limited to supportive care, i.e. safeguarding hemodynamics, and respiration. Maintaining adequate tissue oxygenation is a principal target. Starting enteral nutrition within 36 hours of admission to an intensive care unit has reduced infectious complications. [1]

Prognosis [ edit ]

Mortality, though it has lessened to a limited degree, at least in developed countries with timely access to initial and tertiary care, varies where the chance of survival is diminished as the number of organs involved increases. Mortality in MODS from septic shock (which itself has a high mortality of 25-50%), and from multiple traumas, especially if not rapidly treated, appear to be especially severe. If more than one organ system is affected, the mortality rate is still higher, and this is especially the case when five or more systems or organs are affected. Old age is a risk factor in and of itself, and immunocompromised patients, such as with cancer or AIDS or a transplant, are at risk. Prognosis must take into account any co-morbidities the patient may have, their past and current health status, any genetic or environmental vulnerabilities they have, the nature and type of the illness or injury (as an example, data from COVID-19 is still being analyzed, whereas other cases from long-existing illnesses are much better understood), and any resistance to drugs used to treat microbial infections or any hospital-acquired co-infection. Earlier and aggressive treatment, the use of experimental treatments, or at least modern tools such as ventilators, ECMO, dialysis, bypass, and transplantation, especially at a trauma center, may improve outcomes in certain cases, but this depends in part on speedy and affordable access to high-quality care, which many areas lack. Measurements of lactate, cytokines, albumin and other proteins, urea, blood oxygen and carbon dioxide levels, insulin, and blood sugar, adequate hydration, constant monitoring of vital signs, good communication within and between facilities and staff, and adequate staffing, training, and charting are important in MODS, as in any serious illness. [6] [7] [8] [9] [10]

In patients with sepsis, septic shock, or multiple organ dysfunction syndrome that is due to major trauma, the rs1800625 polymorphism is a functional single nucleotide polymorphism, a part of the receptor for advanced glycation end products (RAGE) transmembrane receptor gene (of the immunoglobulin superfamily) and confers host susceptibility to sepsis and MODS in these patients. [11]

History [ edit ]

For many years, some patients were loosely classified as having sepsis or the sepsis syndrome. In more recent years, these concepts have been refined – so that there are specific definitions of sepsis – and two new concepts have been developed: the SIRS and MODS. [1]

References [ edit ]

  1. ^ abcdefghijk Irwin, Richard S.; Rippe, James M. (2003). Irwin and Rippe’s Intensive Care Medicine. Lippincott Williams & Wilkins. ISBN978-0-7817-3548-3 . [page needed]
  2. ^
  3. Matsuda, Naoyuki; Hattori, Yuichi (2006). «Systemic Inflammatory Response Syndrome (SIRS): Molecular Pathophysiology and Gene Therapy». Journal of Pharmacological Sciences. 101 (3): 189–198. doi: 10.1254/jphs.crj06010x . PMID16823257.
  4. ^
  5. Deitch, Edwin A. (1 June 1989). «Simple Intestinal Obstruction Causes Bacterial Translocation in Man». Archives of Surgery. 124 (6): 699–701. doi:10.1001/archsurg.1989.01410060065013. PMID2730322.
  6. ^
  7. McIlroy, Daniel J.; Jarnicki, Andrew G.; Au, Gough G.; Lott, Natalie; Smith, Doug W.; Hansbro, Philip M.; Balogh, Zsolt J. (December 2014). «Mitochondrial DNA neutrophil extracellular traps are formed after trauma and subsequent surgery». Journal of Critical Care. 29 (6): 1133.e1–1133.e5. doi: 10.1016/j.jcrc.2014.07.013 . PMID25128442.
  8. ^
  9. «MULTIPLE ORGAN FAILURE». ABC Australia. 7 August 2014.
  10. ^
  11. Watson, R. Scott; Crow, Sheri S.; Hartman, Mary E.; Lacroix, Jacques; Odetola, Folafoluwa O. (2017). «Epidemiology and outcomes of pediatric multiple organ dysfunction syndrome (MODS)». Pediatric Critical Care Medicine. 18 (3 Suppl 1): S4–S16. doi:10.1097/PCC.0000000000001047. PMC5334773 . PMID28248829.
  12. ^
  13. van Wessem, Karlijn J.P.; Leenen, Luke P.H. (1 January 2018). «Reduction in Mortality Rates of Postinjury Multiple Organ Dysfunction Syndrome: A Shifting Paradigm? A Prospective Population-Based Cohort Study». Shock: Injury, Inflammation, and Sepsis: Laboratory and Clinical Approaches. 49 (1): 33–38. doi:10.1097/SHK.0000000000000938. PMID28682941. S2CID206062912.
  14. ^
  15. Liu, Xiaoli; Hu, Pan; Mao, Zhi; Kuo, Po-Chih; Li, Peiyao; Liu, Chao; Hu, Jie; Li, Deyu; Cao, Desen; Mark, Roger G.; Celi, Leo Anthony; Zhang, Zhengbo; Zhou, Feihu (28 January 2020). «Interpretable Machine Learning Model for Early Prediction of Mortality in Elderly Patients with Multiple Organ Dysfunction Syndrome (MODS): a Multicenter Retrospective Study and Cross Validation». arXiv: 2001.10977 . > : Cite journal requires |journal= (help)
  16. ^
  17. van Breugel, Johanna M. M.; Niemeyer, Menco J. S.; Houwert, Roderick M.; Groenwold, Rolf H. H.; Leenen, Luke P. H.; van Wessem, Karlijn J. P. (December 2020). «Global changes in mortality rates in polytrauma patients admitted to the ICU—a systematic review». World Journal of Emergency Surgery. 15 (1): 55. doi:10.1186/s13017-020-00330-3. PMC7526208 . PMID32998744.
  18. ^
  19. Sapan, Heber Bombang; Paturusi, Idrus; Jusuf, Irawan; Patellongi, Ilhamjaya; Massi, Muh Nasrum; Pusponegoro, Aryono Djuned; Arief, Syafrie Kamsul; Labeda, Ibrahim; Islam, Andi Asadul; Rendy, Leo; Hatta, Mochammad (1 June 2016). «Pattern of cytokine (IL-6 and IL-10) level as inflammation and anti-inflammation mediator of multiple organ dysfunction syndrome (MODS) in polytrauma». International Journal of Burns and Trauma. 6 (2): 37–43. PMC4913232 . PMID27335696.
  20. ^
  21. Zeng, Ling; Du, Juan; Gu, Wei; Zhang, An-qiang; Wang, Hai-yan; Wen, Da-lin; Qiu, Lin; Yang, Xue-tao; Sun, Jian-hui; Zhang, Mao; Hao, Jiang; Jiang, Jian-xin (2015). «Rs1800625 in the receptor for advanced glycation end products gene predisposes to sepsis and multiple organ dysfunction syndrome in patients with major trauma». Critical Care. 19 (1): 6. doi:10.1186/s13054-014-0727-2. PMC4310192 . PMID25572180.
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Further reading [ edit ]

  • The ICU Book by Marino
  • Cecil Textbook of Medicine
  • The Oxford Textbook of Medicine
  • Harrison’s Principles of Internal Medicine

The Organ Transplant Process

A surgeon moves a donated organ to someone whose organ failed. This is an organ transplant. Certain diseases can lead to organ failure. So can injury or birth defects.

How do I get on the organ transplant waiting list?

  1. Get a Referral Your doctor must refer you. A transplant center or program then checks if a transplant makes sense for you.
  2. Gather Information Learn about transplant lists, costs, and recovery. The United Network for Organ Sharing (UNOS) created, What Every Parent Needs to Know (PDF — 5 MB) . It gives you an overview of the process.
  3. Select a Transplant Center Make sure the transplant center meets your needs. Consider its location, if your insurance will pay, how you pay, and if they have support groups. The Organ Procurement and Transplantation Network (OPTN) has a list of member transplant centers.
  4. Make an Appointment Contact the transplant hospital. Set an appointment for them to evaluate you. They will decide if you qualify for a transplant. During the evaluation, ask questions. Learn about that hospital and its transplant team.
  5. Get Listed If you qualify, the transplant team will add you to the OPTN waiting list. The transplant team will contact you in writing about 10 days after they list you. Direct any questions about your waiting list status to your transplant team.

How much will it cost me?

Transplants cost money before, during, and after the surgery. You pay these costs, not the donor.

Your health insurance may cover some costs. Call your insurance company or your employer’s benefits office. Ask what costs your insurance will pay and how.

What do costs include?

  • Lab tests, organ removal, transplant surgeons, and other operating room staff
  • In-hospital stays, getting to and from the transplant hospital for surgery and checkups
  • Recovery, including physical or occupational therapy
  • Medicine (e.g., anti-rejection drugs)

Why should I make a financial plan?

You must pay for any costs that insurance doesn’t cover. Think about how you’ll pay these costs. This may include savings, sale of property, etc.

Who can help me with the plan?

Members of the transplant team, such as the social worker and financial coordinator, can help you develop a plan. They may put you in touch with groups that help pay transplant costs.

How else can the financial coordinator help?

Speak with the financial coordinator before you make financial decisions about your transplant.

They can help you:

  • understand how your insurance company’s benefits apply to transplant surgery;
  • make a plan to pay for your transplant;
  • make a plan for nonmedical costs, such as living expenses;
  • locate sources of funding; and
  • understand bills from hospitals, doctors, pharmacies, and other providers.

Can Medicare or Medicaid help me?

Medicare is a federal program. States operate Medicaid. Both are health insurance programs that may help with your transplant costs.

What is Medicare?

Medicare is for people age 65 or older, people with disabilities, or people who have end-stage renal disease (ESRD).

What will Medicare cover for my transplant?

  • Medicare Part A is free to those who qualify. It covers inpatient hospital care and some nursing home care.
  • Medicare Part B participants pay premiums. Part B covers:
    • outpatient care;
    • doctor bills;
    • some home health care; and
    • prescription medicines including, in some cases, anti-rejection drugs.

    Medicare certifies transplant programs throughout the country. You must use a Medicare-approved transplant facility to receive full Medicare benefits.

    What is Medicaid?

    Medicaid is an insurance program for people with low incomes. The federal government and states fund it. States decide who can get it and what benefits and services they’ll cover.

    What does Medicaid cover for organ transplants?

    Some states’ Medicaid plans cover only transplants done in the state. That is, unless there’s no transplant center for that organ in the state.

    Some states’ Medicaid programs don’t cover transplants. Check what your state Medicaid program covers.

    How can Social Security help?
    Contact your local Social Security office online or call them at 800-772-1213. They can answer questions you have about Medicare or Medicaid. You may qualify for benefits after an organ transplant.

    How does the system match organs?

    The OPTN has rules for how donor organs match to patients on the waiting list.

    This might include how sick a patient is. Their blood type may also be a factor. It depends on the organ.

    What happens after my transplant?

    Doctors will watch your health years after your transplant. Lab tests will be a regular part of your life.

    Talk to your transplant team. Ask:

    • what monitoring you’ll need;
    • what you can have done at home; and
    • what will require visits to the transplant center or other locations.

    How will my body react?

    Your body may reject a transplanted organ or tissue. It sees it as an invader and tries to destroy it.

    Anti-rejection medicine can help. A weak immune system can be slower in defending against germs.

    You may get infections more easily. You may find it harder to recover from infections and illnesses.

    Protect your health. Follow good prevention practices to avoid illness and injury. Get treatment early when you do get sick.

    What medicines can I expect to take?

    You’ll probably need to take several kinds of medicine. You may take some medicines several times a day and others only on certain days. Your medicines or dosages may change.

    Why should I get to know my pharmacist?

    Get to know your pharmacist. They can help you:

    • understand your medicines;
    • manage your medication schedule;
    • explain the effects and side effects of medicines; and
    • recommend tools like timers and organizers. These help you keep track of medications.

    What should I eat, drink, and avoid?


    • High-fiber foods, such as raw vegetables and fruits;
    • Calcium-rich foods, like low-fat dairy products and green, leafy vegetables. You could also take calcium supplements.
    • Foods high in protein, such as meat, poultry, fish, eggs, unsalted nuts, and beans. Protein helps you build muscles and tissue. This helps you heal.


    • Plenty of water, unless your doctor tells you to limit fluids.


    • A lot of salt, processed foods, and snacks. Use herbs and spices to add flavor.
    • Eating too much.

    What kind of exercise can I do?

    Limit exercise and muscle strain when you first return home. Talk with your doctor. They’ll tell you what to expect. And they’ll tell you what activity to limit.

    Most people feel weak after surgery. You’ll have to recover from the operation. You’ll also have to recover from the illness or injury that made you need a transplant.

    When you feel better, exercise will help you regain your strength. You may feel tired at first. Take rest breaks during exercise. Gradually, increase the amount and type of physical activity you enjoy.

    Can I contact my donor’s family?

    You may want to thank your donor’s family. Sometimes donor families want to check on you. Federal law requires transplant centers and Organ Procurement Organizations (OPOs) to protect donors and receiving patients’ privacy. They can arrange for contact between the families when both sides agree. The process may begin with a letter from you to the donor family. Read the guidelines for the first letter in, Contacting My Donor Family.

    Blake was just 16 days old when he received the gift of life. Today, at 14, Blake is a normal, active teenager . who loves sports, loves his team, and whose favorite subject in school is algebra.

    You have the potential to help save lives as a donor. You can start by signing up through your state’s registry.

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